bims-rimeca Biomed News
on RNA methylation in cancer
Issue of 2022–04–10
24 papers selected by
Sk Ramiz Islam, Saha Institute of Nuclear Physics



  1. Mol Cancer. 2022 Apr 09. 21(1): 97
       BACKGROUND: N6-methyladenosine (m6A) RNA modification plays a critical role in various physiological and pathological conditions. However, the role of m6A modification in head and neck squamous cell carcinoma (HNSCC) remains elusive.
    METHODS: In this study, the expression of m6A demethylases was detected by HNSCC tissue microarray. m6A-RNA immunoprecipitation (MeRIP) sequencing and RNA sequencing were used to identify downstream targets of ALKBH5. Comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) was used to explore the m6A "readers". Tumor-infiltrating lymphocytes were analyzed in SCC7-bearing xenografts in C3H mice.
    RESULTS: Here, we demonstrate the downregulation of m6A status and upregulation of two demethylases in HNSCC. Silencing the m6A demethylase alkB homolog 5, RNA demethylase (ALKBH5) suppresses tumor progression in vitro and in vivo. m6A-RNA immunoprecipitation sequencing reveals that ALKBH5 downregulates the m6A modification of DDX58 mRNA. Moreover, RIG-I, encoded by the DDX58 mRNA, reverses the protumorigenic characteristics of ALKBH5. ChIRP-MS demonstrates that HNRNPC binds to the m6A sites of DDX58 mRNA to promote its maturation. ALKBH5 overexpression inhibits RIG-I-mediated IFNα secretion through the IKKε/TBK1/IRF3 pathway. The number of tumor-infiltrating lymphocytes in C3H immunocompetent mice is reduced by ALKBH5 overexpression and restored by IFNα administration. Upregulation of AKLBH5 negatively correlates with RIG-I and IFNα expression in HNSCC patients.
    CONCLUSIONS: These findings unveil a novel mechanism of immune microenvironment regulation mediated by m6A modification through the ALKBH5/RIG-I/IFNα axis, providing a rationale for therapeutically targeting epitranscriptomic modulators in HNSCC.
    Keywords:  ALKBH5; Head and neck squamous cell carcinoma; Interferon alpha; N6-methyladenosine; RIG-I
    DOI:  https://doi.org/10.1186/s12943-022-01572-2
  2. J Oral Pathol Med. 2022 Apr 04. e13292
       BACKGROUND: Oral submucosal fibrosis (OSF) is a precancerous condition that closely related to the habit of chewing betel nut. The OSF patients of 3%-19% may develop cancer, and this probability is increasing year by year. Epigenetics modifications have been reported as part of the pathogenesis of OSF. However, in OSF field, the role and mechanism of arecoline-induced activation of transforming growth factor β (TGF-β) signaling on N6-methyladenosine (m6A) modification remain unclear. In this study, we investigated the effect and mechanism of arecoline on m6A modification.
    METHODS: MeRIP-Seq and RNA-seq were performed in arecoline-stimulated cells. Quantitative polymerase chain reaction and western blot were performed to detect the expression of m6A writers and erasers. CCK-8 and flow cytometry analyses were performed to measure the cell viability and apoptosis.
    RESULTS: m6A level was increased in OSF tissues compared to normal tissues; arecoline promoted the m6A methyltransferase Mettl3 and Mettl14 through TGF-β. MeRIP-seq and RNA-seq analyses found that MYC was the target gene of Mettl14. In addition, Mettl14 silence reversed the effects of arecoline on cell proliferation and apoptosis in Hacat cells.
    CONCLUSION: TGF-β-METTL14-m6A-MYC axis was crucially implicated in arecoline-mediated OSF and may be an effective therapeutic strategy for OSF treatment.
    Keywords:  N6-methyladenosine; TGF-β; arecoline; m6A methyltransferase; oral submucosal fibrosis
    DOI:  https://doi.org/10.1111/jop.13292
  3. Chem Biol Drug Des. 2022 Apr 05.
      A group of RNA methylation enzymes is currently of interest as a new target for cancer therapy. Alpha-ketoglutarate-dependent dioxygenase B (AlkB) homolog 5 (ALKBH5) is an N6 -methyladenosine (m6 A) demethylation enzyme, and by high-throughput screening from pure small molecule compounds, we identified two novel inhibitors, Ena15 and Ena21, against it. Each compound showed either uncompetitive or competitive inhibition for 2-oxoglutarate (2OG). In addition, Ena21 had little inhibitory activity for fat mass and obesity-associated protein (FTO), which is another N6 -methyladenosine demethylation enzyme, while Ena15 enhanced the demethylase activity of FTO. The predicted binding poses of both compounds with the crystal structure of ALKBH5 (PDB ID: 4NRO) were comparable with these observations pertaining to the interaction of the 2OG catalytic site in this enzyme kinetics. Furthermore, either knockdown of ALKBH5 or inhibition with Ena15 or Ena21 inhibited cell proliferation of glioblastoma multiforme-derived cell lines, decreased cell population in the synthesis phase of the cell cycle, increased m6 A RNA level, and stabilized FOXM1 mRNA. Based on these results, Ena15 and Ena21 were found to be potential candidates that might help in further research into the biological function of ALKBH5.
    Keywords:  2-oxoglutarate-dependent dioxygenase; ALKBH5; AlkB homolog 5; N6-methyladenosine RNA demethylation; RNA modifications; cancer therapy; epitranscriptics; epitranscriptome; glioblastoma; high-throughput screening
    DOI:  https://doi.org/10.1111/cbdd.14051
  4. J Healthc Eng. 2022 ;2022 5794422
      We aimed to investigate the bio-functions of METTL3 in promoting breast cancer (BCa) progression via regulating N6-methyladenosine (m6A) modification of EZH2 mRNA. METTL3 levels in 48 cases of BCa and matched paracancerous tissues were detected. In the meantime, METTL3 in BCa patients with different staging or lymphatic metastasis states were examined. Prognosis of the BCa patients was analyzed using Kaplan-Meier estimator. Protein levels of EMT-associated genes and invasive and migratory abilities were evaluated. The binding relationship between EZH2 and METTL3 was analyzed via RIP. Besides, m6A modification of EZH2 mRNA was explored. E-Cadherin level in MCF-7 cells with EZH2 knockdown was tested. Subsequently, ChIP was done to verify the interaction between E-cadherin and EZH2. Regulatory effects of METTL3/E-cadherin axis on EMT and metastasis of BCa were finally determined. METTL3 was upregulated in BCa tissues compared to paracancerous ones. METTL3 was especially higher in T3-T4 BCa or those with lymphatic metastasis. BCa patients expressing high level of METTL3 experienced worse survival. METTL3 was identically upregulated in BCa cell lines. Knockdown of METTL3 in MCF-7 cells attenuated EMT and metastatic abilities. Protein level of EZH2 was downregulated after knockdown of METTL3 in MCF-7 cells, while its mRNA level was not influenced by METTL3. Furthermore, METTL3 was confirmed to interact with EZH2, and m6A modification existed in EZH2 mRNA. Knockdown of EZH2 greatly upregulated mRNA level of E-cadherin, and later, ChIP assay confirmed the interaction between EZH2 and E-cadherin. E-Cadherin could abolish the effects of METTL3 on BCa metastasis and epithelial-mesenchymal transition. METTL3 is upregulated in BCa. It could regulate the protein level of EZH2 through m6A modification to promote EMT and metastasis in BCa cells, thereafter aggravating the progression of BCa.
    DOI:  https://doi.org/10.1155/2022/5794422
  5. Cell Death Discov. 2022 Apr 05. 8(1): 167
      Pathological cardiac hypertrophy is a key contributor in heart failure (HF). Long non-coding RNAs (lncRNAs) and N6-methyladenosine (m6A) modification play a vital role in cardiac hypertrophy respectively. Nevertheless, the interaction between lncRNA and m6A methylase in cardiac hypertrophy is scarcely reported. Here, we constructed a cardiac hypertrophy mouse model by transverse aortic constriction (TAC) surgery and H9c2 cell model by stimulating with AngII. We found that lncRNA MIAT mRNA level, and m6A RNA methylation reading protein Ythdf2 mRNA and protein levels, were significantly increased in the cardiac hypertrophy model both in vivo and vitro. MIAT or Ythdf2 overexpression aggravated cardiac hypertrophy, and vice versa. Through bioinformatics prediction, western blotting, FISH, RNA pull-down, and RIP, we found that MIAT bound to Ythdf2 and regulated its expression. Furthermore, we discovered that Ythdf2 function was a downstream of MIAT in cardiac hypertrophy. Finally, we found that MIAT was a necessary regulator of cardiac hypertrophy due to its regulation of the Ythdf2/PPARα/CPT-1a axis. This study indicated a new hypertrophic signaling pathway: MIAT/Ythdf2/PPARα/CPT-1a. The results provided a new understanding of the MIAT and m6A RNA methylation reading protein, Ythdf2, function and mechanism in cardiac hypertrophy and highlighted the potential therapeutic benefits in the heart.
    DOI:  https://doi.org/10.1038/s41420-022-00977-8
  6. Cell Death Discov. 2022 Apr 08. 8(1): 179
      Osteosarcoma (OS) is a prevalent primary bone sarcoma. Methyltransferase-like 3 (METTL3) is dysregulated in human malignancies. This study explored the mechanism of METTL3 in OS cell proliferation. Our results demonstrated that METTL3 was highly expressed in OS, and correlated with the tumor size, clinical stage, and distant metastasis of OS patients. Higher METTL3 expression indicated poorer prognosis. METTL3 silencing inhibited the malignant proliferation of OS cells, while METTL3 overexpression led to an opposite trend. METTL3 upregulated histone deacetylase 5 (HDAC5) expression in OS cells by increasing the m6A level. HDAC5 reduced the enrichment of H3K9/K14ac on miR-142 promoter, thus suppressing miR-142-5p expression and upregulating armadillo-repeat-containing 8 (ARMC8) level. HDAC5 overexpression or miR-142-5p silencing attenuated the inhibitory effect of METTL3 silencing on OS cell proliferation. Xenograft tumor experiment in nude mice confirmed that METTL3 silencing repressed OS cell proliferation in vivo via the HDAC5/miR-142-5p/ARMC8 axis. Collectively, METTL3-mediated m6A modification facilitated OS cell proliferation via the HDAC5/miR-142-5p/ARMC8 axis.
    DOI:  https://doi.org/10.1038/s41420-022-00926-5
  7. Transcription. 2022 Apr 05. 1-11
      RNA modifications are prevalent among all the classes of RNA, regulate diverse biological processes, and have emerged as a key regulatory mechanism in post-transcriptional control of gene expression. They are subjected to precise spatial and temporal control and shown to be critical for the maintenance of normal development and physiology. For example, m6A modification of mRNA affects stability, recruitment of RNA binding protein (RBP), translation, and splicing. The deposition of m6A on the RNA happens co-transcriptionally, allowing the tight coupling between the transcription and RNA modification machinery. The m6A modification is affected by transcriptional dynamics, but recent insights also suggest that m6A machinery impacts transcription and chromatin signature.
    Keywords:  Epitranscriptome; Transcription; m6A
    DOI:  https://doi.org/10.1080/21541264.2022.2057177
  8. Exp Hematol Oncol. 2022 Apr 05. 11(1): 21
      YT521-B homology domain family member 2 (YTHDF2) is an N6-methyladenosine (m6A)-binding protein that was originally found to regulate the stability of mRNA. Growing evidence has shown that YTHDF2 can participate in multifarious bioprocesses, including embryonic development, immune response, and tumor progression. Furthermore, YTHDF2 is closely associated with the proliferation, apoptosis, invasion, and migration of tumor cells, suggesting its significant role in cancers. YTHDF2 primarily relies on m6A modification to modulate signaling pathways in cancer cells. However, the expression and function of YTHDF2 in human malignancies remain controversial. Meanwhile, the underlying molecular mechanisms of YTHDF2 have not been elucidated. In this review, we principally summarized the biological functions and molecular mechanisms of YTHDF2 in tumors and discussed its prognostic and therapeutic values.
    Keywords:  Cancer; Mechanism; Prognosis; YTHDF2; m6A
    DOI:  https://doi.org/10.1186/s40164-022-00269-y
  9. Front Cell Dev Biol. 2022 ;10 818194
      N6-methyladenosine (m6A) is the product of the most prevalent mRNA modification in eukaryotic cells. Accumulating evidence shows that tumor microenvironment (TME) plays a pivotal role in tumor development. However, the underlying relationship between m6A modification and the TME of a papillary renal cell carcinoma (PRCC) is still unclear. To investigate the relationship between m6A modification and prognosis and immunotherapeutic efficacy for PRCC, we looked for distinct m6A modification patterns based on 23 m6A-related genes. Next, the correlation between m6A modification patterns and TME-related characteristics was investigated. Then, the intersected differentially expressed genes were selected and the scoring system, denoted as m6A score, was established to evaluate m6A modification, prognosis, and immunotherapeutic efficacy. In this study, three distinct m6A expression clusters were identified. Based on the results of immune cell infiltration analysis and functional analysis, carcinogenic pathways, TME-related immune cells, and pathways were identified as well. More importantly, the established m6A score showed good value in predicting clinical outcomes according to results using external cohorts. Specifically, PRCC patients with low m6A score value showed better survival, immunotherapeutic response, and higher tumor mutation burden. Furthermore, immunohistochemistry using PRCC clinical samples from our medical center was carried out and verified our results. In conclusion, this study highlights the underlying correlation between m6A modification and the immune landscape and, hence, enhances our understanding of the TME and improved the therapeutic outlook for PRCC patients.
    Keywords:  immunotherapy; m 6 A; mutation burden; survival; tumor microenvironment
    DOI:  https://doi.org/10.3389/fcell.2022.818194
  10. Front Neurosci. 2022 ;16 739201
      Loss-of-function mutations in the gene that encodes TYRO protein kinase-binding protein (TYROBP) cause Nasu-Hakola disease, a heritable disease resembling Alzheimer's disease (AD). Methylation of N6 methyl-adenosine (m6A) in mRNA plays essential roles in learning and memory. Aberrant m6A methylation has been detected in AD patients and animal models. In the present study, Tyrobp-/- mice showed learning and memory deficits in the Morris water maze, which worsened with age. Tyrobp-/- mice also showed elevated levels of total tau, Ser202/Thr205-phosphorylated tau and amyloid β in the hippocampus and cerebrocortex, which worsened with aging. The m6A methyltransferase components METTL3, METTL14, and WTAP were downregulated in Tyrobp-/- mice, while expression of demethylases that remove the m6A modification (e.g., FTO and ALKBH5) were unaltered. Methylated RNA immunoprecipitation sequencing identified 498 m6A peaks that were upregulated in Tyrobp-/- mice, and 312 m6A peaks that were downregulated. Bioinformatic analysis suggested that most of these m6A peaks occur in sequences near stop codons and 3'-untranslated regions. These findings suggest an association between m6A RNA methylation and pathological TYROBP deficiency.
    Keywords:  ALKBH5; FTO; METTL14; METTL3; MeRIP-seq; Tyrobp–/– mice; WTAP; m6A methylation
    DOI:  https://doi.org/10.3389/fnins.2022.739201
  11. Future Oncol. 2022 Apr 05.
      Background: N6-methyladenosine (m6A) is crucial in cancer and is being intensively studied. Aim: This bibliometric analysis seeks a broad picture of the role of m6A in cancer to guide and broaden future research. Methods: Publications were retrieved from Web of Science Core Collection and PubMed from 2000 to 2021, with keywords 'm6A' and 'cancer', and analyzed in biblioshiny and VOSviewer. Results: A total of 1013 documents were included, and China and the USA were the top countries with close collaboration. Mechanisms and predictive biomarkers of m6A regulator genes were highlighted. Cross-integration of m6A and other research hot spots, including 'immunotherapy', 'hypoxia' and 'polymorphism', were frontiers of m6A in cancer. Conclusion: This bibliometric study offered an updated perspective on m6A in cancer.
    Keywords:  N6-methyladenosine; bibliometric analysis; cancer; epigenetic transcriptomics; m6A
    DOI:  https://doi.org/10.2217/fon-2022-0086
  12. Free Radic Biol Med. 2022 Apr 02. pii: S0891-5849(22)00134-4. [Epub ahead of print]
      Clear cell renal cell carcinoma (ccRCC) is a common kidney malignancy that is characterized by poor prognosis. RNA-binding motif protein 15 (RBM15) has been identified as an oncogene in multiple tumors. Nevertheless, the function and mechanism of RBM15 in ccRCC are not clear. In this study, RBM15 was found to be upregulated in ccRCC cells and tissues. RBM15 enhanced the proliferation, clone formation, migration, invasion and epithelial-interstitial transition of ccRCC cells. Enhanced RBM15 was caused by the abundant histone 3 acetylation modification of the RBM15 promoter induced by EP300/CBP. RBM15 enhanced the stability of CXCL11 mRNA in an m6A-dependent manner. Moreover, RBM15 was found to promote macrophage infiltration and M2 polarization by promoting the secretion of CXCL11 in ccRCC cells in vitro and in vivo. Our findings highlight the function of RBM15 in ccRCC and reveal a novel identified EP300/CBP-RBM15-CXCL11 signaling axis, which promotes ccRCC progression and provides new insight into ccRCC therapy.
    Keywords:  Clear cell renal cell carcinoma; Histone modification; N6-methyladenosine; RBM15
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2022.03.031
  13. Front Genet. 2022 ;13 832677
      Spermatogenesis, an efficient and complex system in male germline development, requires a series of elaborately regulated genetic events in which diploid spermatogonia differentiate into haploid spermatozoa. N6-methyladenosine (m6A) is an important epigenetic RNA modification that occurs during spermatogenesis. ALKBH5 is an m6A eraser and knocking out Alkbh5 increases the level of total m6A methylation and causes male infertility. In this study, comprehensive analyses of MeRIP-seq and RNA-seq data revealed differences between wild-type (WT) and Alkbh5 knockout (KO) mice. In pachytene spermatocytes (PA), 8,151 m6A peaks associated with 9,959 genes were tested from WT and 10,856 m6A peaks associated with 10,016 genes were tested from KO mice. In the round spermatids (RO), 10,271 m6A peaks associated with 10,109 genes were tested from WT mice and 9,559 m6A peaks associated with 10,138 genes were tested from KO mice. The peaks were mainly concentrated in the coding region and the stop codon of the GGAC motif. In addition, enrichment analysis showed significant m6A methylation genes in related pathways in spermatogenesis. Furthermore, we conducted joint analyses of the m6A methylome and RNA transcription, suggesting an m6A regulatory mechanism of gene expression. Finally, seven differentially expressed mRNAs from RNA-seq data in both PA and RO were verified using qPCR. Overall, our study provides new information on m6A modification changes between WT and KO in PA and RO, and may provide new insights into the molecular mechanisms of m6A modification in germ cell development and spermatogenesis.
    Keywords:  m6A methylation; merip sequencing; pachytene spermatocytes; round spermatids; spermatogenesis
    DOI:  https://doi.org/10.3389/fgene.2022.832677
  14. Bioengineered. 2022 Apr;13(4): 9301-9311
      Esophageal squamous cell carcinoma (ESCC) is a deadly malignant tumor that threatens human health. Long noncoding RNA (lncRNA) is widely expressed in eukaryotes and is closely associated with human disease progression. However, its role in ESCC remains incompletely understood. In this study, we analyzed the results of three gene expression omnibus (GEO) databases containing lncRNA expression data of ESCC and normal tissues. The results showed that HCP5 was significantly overexpressed in ESCC tissues, which was further verified in our collected ESCC samples. The functional study suggested that HCP5 knockdown inhibited ESCC cell proliferation and invasion. Regarding the mechanism, HCP5 was able to directly interact with YTHDF1, a N6-methyladenosine (m6A) reader, enhancing the binding of YTHDF1 to m6A-modified HK2 mRNA, leading to increasing HK2 stability, thereby promoting the Warburg effect (aerobic glycolysis) of ESCC cells. The nude mice model showed that the knockdown of HCP5 in vivo remarkably reduced tumor size. Clinically, high HCP5 was positively correlated with larger tumor volume, higher TNM stage and lymph node metastasis. Moreover, ESCC patients with high HCP5 exerted shorter survival time than patients with low HCP5. These findings uncover the importance of HCP5 in human ESCC progression; the turbulence of HCP5/YTHDF1/HK2 axis may be responsible for ESCC carcinogenicity.
    Keywords:  ESCC; HCP5; biomarker; m6A; warburg effect
    DOI:  https://doi.org/10.1080/21655979.2022.2051854
  15. J Cell Physiol. 2022 Apr 06.
      N6-methyladenosine (m6A) is an extremely common and conservative posttranscriptional modification, that can specifically target and regulate the expression or stability of a series of tumor-related genes, thus playing critical roles in the occurrence and development of tumors. c-Myc is an important tumorigenic transcription factor that promotes tumorigenesis and development by mainly regulating the expression of downstream target genes. Increasing evidence shows that m6A modification, as well as abnormal expression and regulation of c-Myc, is critical molecular mechanisms driving tumorigenesis and development. Although more evidence has been uncovered about the individual roles of m6A modification or c-Myc in tumors, the interaction between m6A modification and c-Myc in tumorigenesis and development has not been systematically summarized. Therefore, this review is focused on the mutual regulation between m6A modification and c-Myc expression and stability as well as its roles in tumorigenesis and development. We also summarized the potential value of the interaction between m6A modification and m6A expression and stability in tumor diagnosis and treatment, which provides a specific reference for revealing the mechanism of tumor occurrence and development as well as clinical diagnosis and treatment.
    Keywords:  c-Myc; epigenetic regulation; interaction; m6A modification; tumor progression
    DOI:  https://doi.org/10.1002/jcp.30733
  16. Crit Rev Eukaryot Gene Expr. 2022 ;32(1): 79-98
      Kidney renal clear cell carcinoma (KIRC) is the most common and aggressive subtype of renal cell carcinoma. N6-methyladenosine (m6A) RNA methylation is the most prevalent epigenetic RNA modification. Long non-coding RNAs (lncRNAs) have emerged as a key role in regulating cancer progression. However, little has been learned about the molecular functions of m6A-related lncRNAs in KIRC. The prognostic value of m6A-related ln-cRNAs was investigated in KIRC samples downloaded from The Cancer Genome Atlas (TCGA) dataset. The m6A-related lncRNAs were further screen out by Pearson correlation test. Then, 27 m6A-related lncRNAs were confirmed as potential prognostic factors through univariate Cox regression analysis. They were entered into Lasso and multivariate Cox regression to build a m6A-related lncRNA prognostic signature, including 14 m6A-related lncRNAs determined as independent prognostic factors. Additionally, a risk score calculated according to the prognostic model could divide KIRC patients into low- and high-risk groups depending on median risk score as cut-off. A prognostic nomogram, derived from the prognostic model and integrating clinical characteristics of patients, was constructed. Three distinct clusters were identified with different immune signatures through consensus clustering analysis according to the expression pattern of m6A-related lncRNAs. Twenty-seven prognostic m6A-related lncRNAs were determined as prognostic lncRNAs from TCGA-KIRC cohort. The m6A-related lncRNA prognostic signature containing 14 independent prognostic lncRNAs exhibited good accuracy in predicting overall survival of KIRC patients. We correlated the three distinct clusters with immune infiltration signature of KIRC for the first time. We found that the worse prognosis of cluster2 was probably mediated by immune evasion. In summary, our study identified a m6A-related lncRNAs prognostic signature which had great clinical value in prognosis assessment. We classified TCGA-KIRC samples into three clusters with distinct immune signatures, which could be considered as potential targets of immunotherapy for KIRC treatment in the future.
    DOI:  https://doi.org/10.1615/CritRevEukaryotGeneExpr.2021039325
  17. Front Endocrinol (Lausanne). 2022 ;13 853857
       Objective: The objective of this study was to reveal the potential crosstalk between immune infiltration and N6- methyladenosine (m6A) modification in the placentas of patients with gestational diabetes mellitus (GDM), and to construct a model for the diagnosis of GDM.
    Methods: We analyzed imbalanced immune infiltration and differentially expressed m6A-related genes (DMRGs) in the placentas of patients with GDM, based on the GSE70493 dataset. An immune-related DMRG signature, with significant classifying power and diagnostic value, was identified using a least absolute shrinkage and selection operator (LASSO) regression. Based on the selected DMRGs, we developed and validated a nomogram model using GSE70493 and GSE92772 as the training and validation sets, respectively.
    Results: Infiltration of monocytes was higher in GDM placentas than in control samples, while the infiltration of macrophages (M1 and M2) in GDM placentas was lower than in controls. A total of 14 DMRGs were strongly associated with monocyte infiltration, seven of which were significant in distinguishing patients with GDM from normal controls. These genes were CD81, CFH, FABP5, GBP1, GNG11, IL1RL1, and SLAMF6. The calibration curve, decision curve, clinical impact curve, and receiver operating characteristic curve showed that the nomogram recognized GDM with high accuracy in both the training and validation sets.
    Conclusions: Our results provide clues that crosstalk between m6A modification and immune infiltration may have implications in terms of novel biomarkers and therapeutic targets for GDM.
    Keywords:  N6-methyladenosine modification; gestational diabetes mellitus; immune infiltration; monocyte; nomogram
    DOI:  https://doi.org/10.3389/fendo.2022.853857
  18. Front Cell Dev Biol. 2022 ;10 807786
      5-Methylcytosine (m5C) is an abundant and highly conserved modification in RNAs. The dysregulation of RNA m5C methylation has been reported in cancers, but the regulatory network in ovarian cancer of RNA m5C methylation-related genes and its implication in metabolic regulation remain largely unexplored. In this study, RNA-sequencing data and clinical information of 374 ovarian cancer patients were downloaded from The Cancer Genome Atlas database, and a total of 14 RNA m5C regulators were included. Through unsupervised consensus clustering, two clusters with different m5C modification patterns were identified with distinct survivals. According to enrichment analyses, glycosaminoglycan and collagen metabolism-related pathways were specifically activated in cluster 1, whereas fatty acid metabolism-related pathways were enriched in cluster 2, which had better overall survival (OS). Besides the metabolism heterogeneity, the higher sensitivity to platinum and paclitaxel in cluster 2 can further explain the improved OS. Ultimately, a least absolute shrinkage and selection operator prediction model formed by ALYREF, NOP2, and TET2 toward OS was constructed. In conclusion, distinct m5C modification pattern exhibited metabolism heterogeneity, different chemotherapy sensitivity, and consequently survival difference, providing evidence for risk stratification.
    Keywords:  5-methylcytosine; LASSO cox regression; RNA modification; metabolism heterogeneity; ovarian cancer
    DOI:  https://doi.org/10.3389/fcell.2022.807786
  19. Mol Cancer. 2022 Apr 02. 21(1): 93
       BACKGROUND: Circular RNAs (circRNAs) regulate various biological activities and have been shown to play crucial roles in hepatocellular carcinoma (HCC) progression. However, only a few coding circRNAs have been identified in cancers, and their roles in HCC remain elusive. This study aimed to identify coding circRNAs and explore their function in HCC.
    METHODS: CircMAP3K4 was selected from the CIRCpedia database. We performed a series of experiments to determine the characteristics and coding capacity of circMAP3K4. We then used in vivo and in vitro assays to investigate the biological function and mechanism of circMAP3K4 and its protein product, circMAP3K4-455aa, in HCC.
    RESULTS: We found circMAP3K4 to be an upregulated circRNA with coding potential in HCC. IGF2BP1 recognized the circMAP3K4 N6-methyladenosine modification and promoted its translation into circMAP3K4-455aa. Functionally, circMAP3K4-455aa prevented cisplatin-induced apoptosis in HCC cells by interacting with AIF, thus protecting AIF from cleavage and decreasing its nuclear distribution. Moreover, circMAP3K4-455aa was degraded through the ubiquitin-proteasome E3 ligase MIB1 pathway. Clinically, a high level of circMAP3K4 is an independent prognostic factor for adverse overall survival and adverse disease-free survival of HCC patients.
    CONCLUSIONS: CircMAP3K4 is a highly expressed circRNA in HCC. Driven by m6A modification, circMAP3K4 encoded circMAP3K4-455aa, protected HCC cells from cisplatin exposure, and predicted worse prognosis of HCC patients. Targeting circMAP3K4-455aa may provide a new therapeutic strategy for HCC patients, especially for those with chemoresistance. CircMAP3K4 is a highly expressed circRNA in HCC. Driven by m6A modification, IGF2BP1 facilitates circMAP3K4 peptide translation, then the circMAP3K4 peptide inhibits AIF cleavage and nuclear distribution, preventing HCC cells from cell death under stress and promoting HCC progression.
    Keywords:  AIF; Hepatocellular carcinoma; MIB1; N6-methyadenosine; Translation; circMAP3K4
    DOI:  https://doi.org/10.1186/s12943-022-01537-5
  20. J Oncol. 2022 ;2022 1531474
      Aberrant 5-methylcytidine (m5C) modification plays an essential role in the progression of different cancers. More and more researchers are focusing on developing a lncRNA-based risk model to assess the clinical prognosis of cancer patients. However, the impact of m5C-related lncRNAs on the prognosis of patients with uterine corpus endometrial carcinoma (UCEC), as well as the immune microenvironment of UCEC, remains unclear. Here, we comprehensively analyzed the predictive value of m5C-associated lncRNAs in UCEC and their association with the tumor immune microenvironment, according to the information extracted from the TCGA-UCEC dataset. We identified a total of 32 m5C-associated lncRNAs that were significantly correlated with the prognosis of UCEC patients. Two molecular subtypes were determined by consensus clustering analysis of these 32 m5C-associated prognostic lncRNAs. Further data showed that cluster 1 was associated with poor clinical prognosis, advanced tumor grade, higher PD-L1 expression levels, higher ESTIMATEScore, and higher immuneScore, as well as the immune cell infiltration. Then, 17 m5C-associated lncRNAs with prognostic values were obtained using LASSO regression analysis. And a risk model was constructed based on these 17 lncRNAs. It was revealed that the risk model could be used as an independent factor for UCEC prognosis. In addition, patients with UCEC in the high-risk group had higher tumor grades and immune scores. The risk model based on m5C-related lncRNAs was also closely associated with infiltrating immune cells. In conclusion, our study elucidated the crucial roles of the identified m5C-related lncRNAs in the UCEC patients' prognoses, as well as in the immune microenvironment in UCEC. The results suggest that the components of risk models based on the m5C-related lncRNAs may serve as important mediators of the immune microenvironment in UCEC.
    DOI:  https://doi.org/10.1155/2022/1531474
  21. Pathol Res Pract. 2022 Apr 01. pii: S0344-0338(22)00113-3. [Epub ahead of print]233 153870
       BACKGROUND: The study was aimed to find promising targets for cancer therapy involved in the tumorigenesis of hepatocellular carcinoma (HCC).
    METHODS: Identification of STEAP4 in HCC between GSE54503 and TCGA datasets by performing RNA-seq. The STEAP4 mRNA expression level was determined by qRT-PCR. DNA methylation was measured by MSP and BSP. Besides, the effect of STEAP4 tumorigenesis was determined by in vivo experiments. The function of STEAP4 on methylation was further assessed by 5-Aza‑dC, a demethylating agent.
    RESULTS: Reduced STEAP4 expression was found in HCC tissues. Promoter region methylation correlated with the downregulated expression of STEAP4. STEAP4 inhibited the proliferation and metastasis of HCC cells. Re-expression of STEAP4 was induced 5-Aza‑dC. STEAP4 mediated the biological effects of HCC cells through PI3K/AKT/mTOR pathway inhibition.
    CONCLUSIONS: Our findings indicate that STEAP4 functions as a suppressor gene in HCC, and hypermethylation is a driving factor in cancer progression.
    Keywords:  Hepatocellular carcinoma; Methylation; Progression; STEAP4
    DOI:  https://doi.org/10.1016/j.prp.2022.153870
  22. Biomark Res. 2022 Apr 08. 10(1): 19
      Heterogeneous nuclear ribonucleoproteins C (HnRNP C) is part of the hnRNP family of RNA-binding proteins. The relationship between hnRNP C and cancers has been extensively studied, and dysregulation of hnRNP C has been found in many cancers. According to existing public data, hnRNP C could promote the maturation of new heterogeneous nuclear RNAs (hnRNA s, also referred to as pre-mRNAs) into mRNAs and could stabilize mRNAs, controlling their translation. This paper reviews the regulation and dysregulation of hnRNP C in cancers. It interacts with some cancer genes and other biological molecules, such as microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and double-stranded RNAs (dsRNAs). Even directly binds to them. The effects of hnRNP C on biological processes such as alternative cleavage and polyadenylation (APA) and N6-methyladenosine (m6A) modification differ among cancers. Its main function is regulating stability and level of translation of cancer genes, and the hnRNP C is regarded as a candidate biomarker and might be valuable for prognosis evaluation.
    Keywords:  Cancers; HnRNP C; Molecular interactions; RNA-binding protein
    DOI:  https://doi.org/10.1186/s40364-022-00366-4
  23. Cell Death Discov. 2022 Apr 08. 8(1): 176
      The underlying mechanisms of methionine adenosyltransferase 2 A (MAT2A)-mediated cervical cancer progression under nutrient stress are largely elusive. Therefore, our study aims to investigate molecular mechanism by which MAT2A-indcued cervical oncogenesis. The interaction between MAT2A and programmed cell death protein 6 (PDCD6) in cervical cancer cell lines was detected by immunoprecipitation, immunoblotting and mass spectrometric analysis. A panel of inhibitors that are linked to stress responsive kinases were utilized to detect related pathways by immunoblotting. Cell proliferation and apoptosis were investigated by CCK-8 and flow cytometry. Apoptosis related protein level of Bcl-2, Bax and Caspase-3 was also analyzed in cells with PDCD6 K90 methylation mutation. The association between MAT2A and PDCD6 was detected by immunohistochemistry and clinicopathological characteristics were further analyzed. We found that the interaction between MAT2A and PDCD6 is mediated by AMPK activation and facilitates PDCD6 K90 methylation and further promotes protein stability of PDCD6. Physiologically, expression of PDCD6 K90R leads to increased apoptosis and thus suppresses growth of cervical cancer cells under glucose deprivation. Furthermore, the clinical analysis indicates that the MAT2A protein level is positively associated with the PDCD6 level, and the high level of PDCD6 significantly correlates with poor prognosis and advanced stages of cervical cancer patients. We conclude that MAT2A facilitates PDCD6 methylation to promote cervical cancer growth under glucose deprivation, suggesting the regulatory role of MAT2A in cellular response to nutrient stress and cervical cancer progression.
    DOI:  https://doi.org/10.1038/s41420-022-00987-6
  24. Int J Gen Med. 2022 ;15 3525-3540
       Background: The prognostic value of m6A-related genes in hepatocellular carcinoma (HCC) and its correlation with the immune microenvironment still requires further investigation.
    Methods: Consensus clustering by m6A related genes was used to classify 374 patients with HCC from The Cancer Genome Atlas (TCGA) database. Then we performed the least absolute shrinkage and selection operator (LASSO) to construct the m6A related genes model. The International Cancer Genome Consortium (ICGC) and Gene Expression Omnibus (GEO) datasets were used to verify and evaluate the model. ESTIMATE, CIBERSORTx, the expression levels of immune checkpoint genes, and TIDE were used to investigate the tumor microenvironment (TME) and the response to immunotherapy. Gene set enrichment analyses (GSEA), tumor-associated macrophages (TAMs), and gene-drug sensitivity were also analyzed.
    Results: By expression value and regression coefficient of five m6A related genes, we constructed the risk score of each patient. The patients with a higher risk score had a considerably poorer prognosis in the primary and validated cohort. For further discussing TME and the response to immunotherapy, we divided the entire set into two groups based on the risk score. Our findings implied that the tumor-infiltrating lymphocytes (TILs) were proportional to the risk scores, which seemed to contradict that patients with higher scores had a poor prognosis. Further, we found that the high-risk group had higher expression of PD-L1, CTLA-4, and PDCD1, indicating immune dysfunction, which may be a fundamental reason for poor prognosis. This was further reinforced by the fact that the low-risk group responded better than the high-risk group to monotherapy and combination therapy.
    Conclusion: The m6A related risk score is a new independent prognostic factor that correlates with immunotherapy response. It can provide a new therapeutic strategy for improving individual immunotherapy in HCC.
    Keywords:  N6-methyladenine; drug sensitivity; hepatocellular carcinoma; immunotherapy; tumor immune microenvironment
    DOI:  https://doi.org/10.2147/IJGM.S351815