bims-ectoca Biomed News
on Epigenetic control of tolerance in cancer
Issue of 2022‒01‒23
ten papers selected by
Ankita Daiya
BITS Pilani


  1. Pharmaceutics. 2022 Jan 16. pii: 209. [Epub ahead of print]14(1):
      The dysregulation of gene expression is a critical event involved in all steps of tumorigenesis. Aberrant histone and non-histone acetylation modifications of gene expression due to the abnormal activation of histone deacetylases (HDAC) have been reported in hematologic and solid types of cancer. In this sense, the cancer-associated epigenetic alterations are promising targets for anticancer therapy and chemoprevention. HDAC inhibitors (HDACi) induce histone hyperacetylation within target proteins, altering cell cycle and proliferation, cell differentiation, and the regulation of cell death programs. Over the last three decades, an increasing number of synthetic and naturally derived compounds, such as dietary-derived products, have been demonstrated to act as HDACi and have provided biological and molecular insights with regard to the role of HDAC in cancer. The first part of this review is focused on the biological roles of the Zinc-dependent HDAC family in malignant diseases. Accordingly, the small-molecules and natural products such as HDACi are described in terms of cancer therapy and chemoprevention. Furthermore, structural considerations are included to improve the HDACi selectivity and combinatory potential with other specific targeting agents in bifunctional inhibitors and proteolysis targeting chimeras. Additionally, clinical trials that combine HDACi with current therapies are discussed, which may open new avenues in terms of the feasibility of HDACi's future clinical applications in precision cancer therapies.
    Keywords:  HDAC inhibitors; PROTAC; bifunctional inhibitors; cancer; chemoprevention; clinical trials; dietary-derived inhibitors; epigenetic; histone deacetylases
    DOI:  https://doi.org/10.3390/pharmaceutics14010209
  2. Bioorg Chem. 2022 Jan 12. pii: S0045-2068(22)00009-8. [Epub ahead of print]120 105604
      Overexpression of histone deacetylases (HDACs) are observed in different types of cancers, but histone deacetylase inhibitors (HDACIs) have not shown significant efficacy as monotherapy against solid tumors. Recently, studies demonstrated that it is promising to combine HDACIs with DNA damage agents to improve DNA damage level to gain better effect on treating solid tumor. Harmine has been demonstrated to cause DNA damage by intercalating DNA. Therefore, we designed a series of harmine-based inhibitors targeting HDAC and DNA with multi-target strategy, the most potential compound 27 could bind to DNA and cause DNA damage. Furthermore 27 caused cells apoptosis through p53 signaling pathway, and exhibited significant anti-proliferation effects against HCT-116 cells (IC50 = 1.41 μM). As a DNA damage agent, 27 displayed low toxicity in normal cells. Compound 27 was demonstrated as a dual inhibitor targeting HDAC (HDAC1 IC50 = 0.022 μM and HDAC6 IC50 = 0.45 μM) and DNA, and had the potential in the treatment of solid tumor.
    Keywords:  Cancer; DNA; DNA damage; HDAC; Harmine
    DOI:  https://doi.org/10.1016/j.bioorg.2022.105604
  3. Cell Rep. 2022 Jan 18. pii: S2211-1247(21)01781-2. [Epub ahead of print]38(3): 110269
      Cells are complex systems in which many functions are performed by different genetically defined and encoded functional modules. To systematically understand how these modules respond to drug or genetic perturbations, we develop a functional module states framework. Using this framework, we (1) define the drug-induced transcriptional state space for breast cancer cell lines using large public gene expression datasets and reveal that the transcriptional states are associated with drug concentration and drug targets, (2) identify potential targetable vulnerabilities through integrative analysis of transcriptional states after drug treatment and gene knockdown-associated cancer dependency, and (3) use functional module states to predict transcriptional state-dependent drug sensitivity and build prediction models for drug response. This approach demonstrates a similar prediction performance as approaches using high-dimensional gene expression values, with the added advantage of more clearly revealing biologically relevant transcriptional states and key regulators.
    Keywords:  cell states; drug response prediction; functional states; machine learning; target prediction
    DOI:  https://doi.org/10.1016/j.celrep.2021.110269
  4. Cell Mol Biol Lett. 2022 Jan 15. 27(1): 7
      Canonical Wnt/β-catenin signaling is a complex cell-communication mechanism that has a central role in the progression of various cancers. The cellular factors that participate in the regulation of this signaling are still not fully elucidated. Lysine acetylation is a significant protein modification which facilitates reversible regulation of the target protein function dependent on the activity of lysine acetyltransferases (KATs) and the catalytic function of lysine deacetylases (KDACs). Protein lysine acetylation has been classified into histone acetylation and non-histone protein acetylation. Histone acetylation is a kind of epigenetic modification, and it can modulate the transcription of important biological molecules in Wnt/β-catenin signaling. Additionally, as a type of post-translational modification, non-histone acetylation directly alters the function of the core molecules in Wnt/β-catenin signaling. Conversely, this signaling can regulate the expression and function of target molecules based on histone or non-histone protein acetylation. To date, various inhibitors targeting KATs and KDACs have been discovered, and some of these inhibitors exert their anti-tumor activity via blocking Wnt/β-catenin signaling. Here, we discuss the available evidence in understanding the complicated interaction of protein lysine acetylation with Wnt/β-catenin signaling, and lysine acetylation as a new target for cancer therapy via controlling this signaling.
    Keywords:  Canonical Wnt/β-catenin signaling; Interaction; Molecular mechanisms; Protein lysine acetylation; Therapy
    DOI:  https://doi.org/10.1186/s11658-021-00305-5
  5. Int J Mol Sci. 2022 Jan 06. pii: 589. [Epub ahead of print]23(2):
      Epigenetic abnormalities affect tumor progression, as well as gene expression and function. Among the diverse epigenetic modulators, the histone methyltransferase G9a has been focused on due to its role in accelerating tumorigenesis and metastasis. Although epigenetic dysregulation is closely related to tumor progression, reports regarding the relationship between G9a and its possible downstream factors regulating breast tumor growth are scarce. Therefore, we aimed to verify the role of G9a and its presumable downstream regulators during malignant progression of breast cancer. G9a-depleted MCF7 and T47D breast cancer cells exhibited suppressed motility, including migration and invasion, and an improved response to ionizing radiation. To identify the possible key factors underlying these effects, microarray analysis was performed, and a TGF-β superfamily member, BMP5, was selected as a prominent target gene. It was found that BMP5 expression was markedly increased by G9a knockdown. Moreover, reduction in the migration/invasion ability of MCF7 and T47D breast cancer cells was induced by BMP5. Interestingly, a G9a-depletion-mediated increase in BMP5 expression induced the phosphorylation of Smad proteins, which are the intracellular signaling mediators of BMP5. Accordingly, we concluded that the observed antitumor effects may be based on the G9a-depletion-mediated increase in BMP5 expression and the consequent facilitation of Smad protein phosphorylation.
    Keywords:  BMP5; G9a; breast cancer; epigenetics
    DOI:  https://doi.org/10.3390/ijms23020589
  6. Biochem Biophys Res Commun. 2022 Jan 11. pii: S0006-291X(22)00031-6. [Epub ahead of print]592 99-105
      long non-coding RNAs (lncRNAs), as tumor suppressors or oncogenes, have been identified to play key roles in tumorigenesis. The present study explored the roles and potential mechanisms of LINC00960 in osteosarcoma (OS). In vitro study showed that silencing LINC00960 inhibited proliferation, migration and invasion of 143B and MG63. In vivo study demonstrated that knockdown of LINC00960 repressed tumor growth. Further investigation revealed that LINC00960 could regulate SALL4 by sponging miR-107 to promote the progression of OS. Together, LINC00960 is a tumor oncogene in the development and prognosis of OS, which may be a new therapeutic target for OS.
    Keywords:  LINC00960; Osteosarcoma; SALL4; miR-107
    DOI:  https://doi.org/10.1016/j.bbrc.2022.01.017
  7. Anticancer Drugs. 2022 Jan 17.
      Osteosarcoma is the most common primary malignant bone tumour in children and teenagers, and it is characterised by drug resistance and high metastatic potential. Increasing studies have highlighted the critical roles of long noncoding RNAs (lncRNAs) as oncogenes or tumour suppressors as well as new biomarkers and therapeutic targets in osteosarcoma. The growth arrestspecific 5 (GAS5) lncRNA can function as a tumour suppressor in several cancers. The present study aimed to validate GAS5 and other chemoresistanceassociated lncRNAs as biomarkers in a cohort of primary osteosarcoma samples, to obtain predictive information on resistance or sensitivity to treatment. The GAS5 and a panel of lncRNAs related to chemoresistance [SNGH1, FOXD2-AS1, deleted in lymphocytic leukemia (DLEU2) and LINC00963] were evaluated in a cohort of osteosarcoma patients enrolled at the Careggi University Hospital. Total RNA was extracted from formalin-fixed paraffin-embedded (FFPE) tissue sections and the expression levels of the lncRNAs were quantified by qPCR. A bioinformatic analysis on deposited RNA-seq data was performed to validate the qPCR results. Clustering analysis shows that GAS5 could be linked to the expression of isoforms 02 and 04 of the lncRNA DLEU2, whereas the DLEU2 isoform 08 is linked to the lncRNA LINC00963. We found that GAS5 is significantly increased in patients with a good prognosis and is expressed differently between chemosensitive and chemoresistant osteosarcoma patients. However, the results obtained are not concordant with the in-silico analysis performed on the TARGET osteosarcoma dataset. In the future, we would enlarge the case series, including different disease settings.
    DOI:  https://doi.org/10.1097/CAD.0000000000001263
  8. Front Cell Dev Biol. 2021 ;9 814955
      Nucleophagy is an organelle-selective subtype of autophagy that targets nuclear material for degradation. The macroautophagic delivery of micronuclei to the vacuole, together with the nucleus-vacuole junction-dependent microautophagic degradation of nuclear material, were first observed in yeast. Nuclear pore complexes and ribosomal DNA are typically excluded during conventional macronucleophagy and micronucleophagy, indicating that degradation of nuclear cargo is tightly regulated. In mammals, similarly to other autophagy subtypes, nucleophagy is crucial for cellular differentiation and development, in addition to enabling cells to respond to various nuclear insults and cell cycle perturbations. A common denominator of all nucleophagic processes characterized in diverse organisms is the dependence on the core autophagic machinery. Here, we survey recent studies investigating the autophagic processing of nuclear components. We discuss nucleophagic events in the context of pathology, such as neurodegeneration, cancer, DNA damage, and ageing.
    Keywords:  ageing; autophagy; cancer; neurodegeneration; nucleophagy
    DOI:  https://doi.org/10.3389/fcell.2021.814955
  9. Brief Bioinform. 2022 Jan 22. pii: bbab577. [Epub ahead of print]
      Enhancer-promoter interaction (EPI) is a key mechanism underlying gene regulation. EPI prediction has always been a challenging task because enhancers could regulate promoters of distant target genes. Although many machine learning models have been developed, they leverage only the features in enhancers and promoters, or simply add the average genomic signals in the regions between enhancers and promoters, without utilizing detailed features between or outside enhancers and promoters. Due to a lack of large-scale features, existing methods could achieve only moderate performance, especially for predicting EPIs in different cell types. Here, we present a Transformer-based model, TransEPI, for EPI prediction by capturing large genomic contexts. TransEPI was developed based on EPI datasets derived from Hi-C or ChIA-PET data in six cell lines. To avoid over-fitting, we evaluated the TransEPI model by testing it on independent test datasets where the cell line and chromosome are different from the training data. TransEPI not only achieved consistent performance across the cross-validation and test datasets from different cell types but also outperformed the state-of-the-art machine learning and deep learning models. In addition, we found that the improved performance of TransEPI was attributed to the integration of large genomic contexts. Lastly, TransEPI was extended to study the non-coding mutations associated with brain disorders or neural diseases, and we found that TransEPI was also useful for predicting the target genes of non-coding mutations.
    Keywords:  Transformer; chromatin structure; enhancer-promoter interaction; non-coding mutation
    DOI:  https://doi.org/10.1093/bib/bbab577
  10. Cell Death Differ. 2022 Jan 20.
      The histone variant H2AZ is overexpressed in diverse cancer types where it facilitates the accessibility of transcriptional regulators to the promoters of cell cycle genes. However, the molecular basis for its dysregulation in cancer remains unknown. Here, we report that glioblastomas (GBM) and glioma stem cells (GSCs) preferentially overexpress H2AZ for their proliferation, stemness and tumorigenicity. Chromatin accessibility analysis of H2AZ2 depleted GSC revealed that E2F1 occupies the enhancer region within H2AZ2 gene promoter, thereby activating H2AZ2 transcription. Exploration of other H2AZ2 transcriptional activators using a customized "anti-H2AZ2" query signature for connectivity map analysis identified STAT3. Co-targeting E2F and STAT3 synergistically reduced the levels of H2AZ, histone 3 lysine 27 acetylation (H3K27ac) and cell cycle gene transcription, indicating that E2F1 and STAT3 synergize to activate H2AZ gene transcription in GSCs. Remarkably, an E2F/STAT3 inhibitor combination durably suppresses GSC tumorigenicity in an orthotopic GBM xenograft model. In glioma patients, high STAT3 signaling is associated with high E2F1 and H2AZ2 expression. Thus, GBM has uniquely opted the use of E2F1- and STAT3-containing "enhanceosomes" that integrate multiple signaling pathways to achieve H2AZ gene activation, supporting a translational path for the E2F/STAT3 inhibitor combination to be applied in GBM treatment.
    DOI:  https://doi.org/10.1038/s41418-021-00926-5