bims-ectoca Biomed News
on Epigenetic control of tolerance in cancer
Issue of 2022–05–01
twelve papers selected by
Ankita Daiya, Birla Institute of Technology and Science



  1. Front Genet. 2022 ;13 860924
      KDM4 proteins are a subfamily of histone demethylases that target the trimethylation of lysines 9 and 36 of histone H3, which are associated with transcriptional repression and elongation respectively. Their deregulation in cancer may lead to chromatin structure alteration and transcriptional defects that could promote malignancy. Despite that KDM4 proteins are promising drug targets in cancer therapy, only a few drugs have been described as inhibitors of these enzymes, while studies on natural compounds as possible inhibitors are still needed. Natural compounds are a major source of biologically active substances and many are known to target epigenetic processes such as DNA methylation and histone deacetylation, making them a rich source for the discovery of new histone demethylase inhibitors. Here, using transcriptomic analyses we determined that the KDM4 family is deregulated and associated with a poor prognosis in multiple neoplastic tissues. Also, by molecular docking and molecular dynamics approaches, we screened the COCONUT database to search for inhibitors of natural origin compared to FDA-approved drugs and DrugBank databases. We found that molecules from natural products presented the best scores in the FRED docking analysis. Molecules with sugars, aromatic rings, and the presence of OH or O- groups favor the interaction with the active site of KDM4 subfamily proteins. Finally, we integrated a protein-protein interaction network to correlate data from transcriptomic analysis and docking screenings to propose FDA-approved drugs that could be used as multitarget therapies or in combination with the potential natural inhibitors of KDM4 enzymes. This study highlights the relevance of the KDM4 family in cancer and proposes natural compounds that could be used as potential therapies.
    Keywords:  KDM4 inhibitor; cancer; drug discovery; epigenetics (chromatin remodeling); natural compounds; structural biology
    DOI:  https://doi.org/10.3389/fgene.2022.860924
  2. Cell Commun Signal. 2022 Apr 28. 20(1): 57
      The epithelial-mesenchymal transition (EMT) is a vital driver of tumor progression. It is a well-known and complex trans-differentiation process in which epithelial cells undergo morphogenetic changes with loss of apical-basal polarity, but acquire spindle-shaped mesenchymal phenotypes. Lysine acetylation is a type of protein modification that favors reversibly altering the structure and function of target molecules via the modulation of lysine acetyltransferases (KATs), as well as lysine deacetylases (KDACs). To date, research has found that histones and non-histone proteins can be acetylated to facilitate EMT. Interestingly, histone acetylation is a type of epigenetic regulation that is capable of modulating the acetylation levels of distinct histones at the promoters of EMT-related markers, EMT-inducing transcription factors (EMT-TFs), and EMT-related long non-coding RNAs to control EMT. However, non-histone acetylation is a post-translational modification, and its effect on EMT mainly relies on modulating the acetylation of EMT marker proteins, EMT-TFs, and EMT-related signal transduction molecules. In addition, several inhibitors against KATs and KDACs have been developed, some of which can suppress the development of different cancers by targeting EMT. In this review, we discuss the complex biological roles and molecular mechanisms underlying histone acetylation and non-histone protein acetylation in the control of EMT, highlighting lysine acetylation as potential strategy for the treatment of cancer through the regulation of EMT. Video Abstract.
    Keywords:  Epithelial-mesenchymal transition; Histone; Lysine acetylation; Non-histone protein; Therapy
    DOI:  https://doi.org/10.1186/s12964-022-00870-y
  3. BMC Bioinformatics. 2022 Apr 26. 23(1): 151
       BACKGROUND: Histone Mark Modifications (HMs) are crucial actors in gene regulation, as they actively remodel chromatin to modulate transcriptional activity: aberrant combinatorial patterns of HMs have been connected with several diseases, including cancer. HMs are, however, reversible modifications: understanding their role in disease would allow the design of 'epigenetic drugs' for specific, non-invasive treatments. Standard statistical techniques were not entirely successful in extracting representative features from raw HM signals over gene locations. On the other hand, deep learning approaches allow for effective automatic feature extraction, but at the expense of model interpretation.
    RESULTS: Here, we propose ShallowChrome, a novel computational pipeline to model transcriptional regulation via HMs in both an accurate and interpretable way. We attain state-of-the-art results on the binary classification of gene transcriptional states over 56 cell-types from the REMC database, largely outperforming recent deep learning approaches. We interpret our models by extracting insightful gene-specific regulative patterns, and we analyse them for the specific case of the PAX5 gene over three differentiated blood cell lines. Finally, we compare the patterns we obtained with the characteristic emission patterns of ChromHMM, and show that ShallowChrome is able to coherently rank groups of chromatin states w.r.t. their transcriptional activity.
    CONCLUSIONS: In this work we demonstrate that it is possible to model HM-modulated gene expression regulation in a highly accurate, yet interpretable way. Our feature extraction algorithm leverages on data downstream the identification of enriched regions to retrieve gene-wise, statistically significant and dynamically located features for each HM. These features are highly predictive of gene transcriptional state, and allow for accurate modeling by computationally efficient logistic regression models. These models allow a direct inspection and a rigorous interpretation, helping to formulate quantifiable hypotheses.
    Keywords:  Epigenetics; Gene expression regulation; Histone modifications; Interpretability
    DOI:  https://doi.org/10.1186/s12859-022-04687-x
  4. Anal Chim Acta. 2022 May 08. pii: S0003-2670(22)00332-4. [Epub ahead of print]1206 339761
      Irinotecan (Iri) is a key drug to treat metastatic colorectal cancer, but its clinical activity is often limited by de novo and acquired drug resistance. Studying the underlying mechanisms of drug resistance is necessary for developing novel therapeutic strategies. In this study, we used both regular and irinotecan-resistant (Iri-resistant) colorectal cell lines as models, and performed single cell mass spectrometry (SCMS) metabolomics studies combined with analyses from cytotoxicity assay, western blot, flow cytometry, quantitative real-time polymerase chain reaction (qPCR), and reactive oxygen species (ROS). Our SCMS results indicate that Iri-resistant cancer cells possess higher levels of unsaturated lipids compared with the regular cancer cells. In addition, multiple protein biomarkers and their corresponding mRNAs of colon cancer stem cells are overexpressed in Iri-resistance cells. Particularly, stearoyl-CoA desaturase 1 (SCD1) is upregulated with the development of drug resistance in Iri-resistant cells, whereas inhibiting the activity of SCD1 efficiently increase their sensitivity to Iri treatment. In addition, we demonstrated that SCD1 directly regulates the expression of ALDH1A1, which contributes to the cancer stemness and ROS level in Iri-resistant cell lines.
    DOI:  https://doi.org/10.1016/j.aca.2022.339761
  5. Chem Asian J. 2022 Apr 30.
      Post-transrational modifications (PTMs) of histones play a key role in epigenetic regulation. Unraveling the roles of each epigenetic mark can provide new insights into their biological mechanisms. On the other hand, it is generally difficult to prepare homogeneously-modified histones/nucleosomes to investigate their specific functions. Therefore, synthetic approaches to acquire precisely mimicked histones/nucleosomes are in great demand, and further development of this research field is anticipated. In this review, synthetic strategies to modify histones/nucleosomes, including cysteine modifications, transformations of dehydroalanine residues and lysine acylation using a catalyst system, are cited. In addition, the functional evaluation of synthetically modified histones/nucleosomes is described.
    Keywords:  epigenetics; histone; nucleosome; post transrational modification; synthetic modification
    DOI:  https://doi.org/10.1002/asia.202200197
  6. Bioinformatics. 2022 Apr 29. pii: btac300. [Epub ahead of print]
       MOTIVATION: Single-cell RNA sequencing (scRNA-seq) technologies have been testified revolutionary for their promotion on the profiling of single-cell transcriptomes at single-cell resolution. Excess zeros due to various technical noises, called dropouts, will mislead downstream analyses. Therefore, it is crucial to have accurate imputation methods to address the dropout problem.
    RESULTS: In this paper, we develop a new dropout imputation method for scRNA-seq data based on multi-objective optimization. Our method is different from existing ones, which assume that the underlying data has a preconceived structure and impute the dropouts according to the information learned from such structure. We assume that the data combines three types of latent structures, including the horizontal structure (genes are similar to each other), the vertical structure (cells are similar to each other), and the low-rank structure. The combination weights and latent structures are learned using multi-objective optimization. And, the weighted average of the observed data and the imputation results learned from the three types of structures are considered as the final result. Comprehensive downstream experiments show the superiority of our method in terms of recovery of true gene expression profiles, differential expression analysis, cell clustering and cell trajectory inference.
    AVAILABILITY: The R package is available at https://github.com/Zhangxf-ccnu/scMOO and https://zenodo.org/record/5785195. The codes to reproduce the downstream analyses in this paper can be found at https://github.com/Zhangxf-ccnu/scMOO_experiments_codes and https://zenodo.org/record/5786211.
    SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.
    DOI:  https://doi.org/10.1093/bioinformatics/btac300
  7. Trends Cell Biol. 2022 Apr 25. pii: S0962-8924(22)00079-4. [Epub ahead of print]
      Most solid cancer-related deaths result from metastasis, a multistep process in which cancer cells exit the primary site, intravasate into the bloodstream, extravasate, and colonize distant organs. Colonization is facilitated by clonal selection and the high phenotypic plasticity of cancer cells that creates reversible switching of cellular states. Cancer cell plasticity leads to intratumor heterogeneity and fitness, yielding cells with molecular and cellular programs that facilitate survival and colonization. While cancer cell plasticity is sometimes limited to the process of epithelial-to-mesenchymal transition (EMT), recent studies have broadened its definition. Plasticity arises from both cell-intrinsic and cell-extrinsic factors and is a major obstacle to efficacious anti-cancer therapies. Here, we discuss the multifaceted notion of cancer cell plasticity associated with metastatic colonization.
    Keywords:  EMT; colonization; dormancy; metastasis; microenvironment; plasticity
    DOI:  https://doi.org/10.1016/j.tcb.2022.03.007
  8. Cell Rep Methods. 2021 Jun 21. 1(2): 100039
      Patient-derived cell lines are often used in pre-clinical cancer research, but some cell lines are too different from tumors to be good models. Comparison of genomic and expression profiles can guide the choice of pre-clinical models, but typically not all features are equally relevant. We present TumorComparer, a computational method for comparing cellular profiles with higher weights on functional features of interest. In this pan-cancer application, we compare ∼600 cell lines and ∼8,000 tumor samples of 24 cancer types, using weights to emphasize known oncogenic alterations. We characterize the similarity of cell lines and tumors within and across cancers by using multiple datum types and rank cell lines by their inferred quality as representative models. Beyond the assessment of cell lines, the weighted similarity approach is adaptable to patient stratification in clinical trials and personalized medicine.
    Keywords:  CCLP; TCGA; cancer genomics; cancer therapy; cell lines; decision support; oncogenic alterations; patient stratification; web application; weighted similarity
    DOI:  https://doi.org/10.1016/j.crmeth.2021.100039
  9. Regen Biomater. 2022 ;9 rbac002
      Magnesium alloy (Mg alloy) has attracted massive attention in the potential applications of cardiovascular stents because of its good biocompatibility and degradability. However, whether and how the Mg alloy induces inflammation in endothelial cells remains unclear. In the present work, we investigated the activation of Yes-associated protein (YAP) upon Mg alloy stimuli and unveiled the transcriptional function in Mg alloy-induced inflammation. Quantitative RT-PCR, western blotting and immunofluorescence staining showed that Mg alloy inhibited the Hippo pathway to facilitate nuclear shuttling and activation of YAP in human coronary artery endothelial cells (HCAECs). Chromatin immunoprecipitation followed sequencing was carried out to explore the transcriptional function of YAP in Mg alloy-derived inflammation. This led to the observation that nuclear YAP further bonded to the promoter region of inflammation transcription factors and co-transcription factors. This binding event activated their transcription and modified mRNA methylation of inflammation-related genes through regulating the expression of N6-methyladenosine modulators (METTL3, METTL14, FTO and WTAP). This then promoted inflammation-related gene expression and aggravated inflammation in HCAECs. In YAP deficiency cells, Mg alloy-induced inflammation was reduced. Collectively, our data suggest that YAP contributes to the Mg alloy-derived inflammation in HCAECs and may provide a potential therapeutic target that alleviates inflammation after Mg alloy stent implantation.
    Keywords:  Yes-associated protein; inflammation; magnesium alloy
    DOI:  https://doi.org/10.1093/rb/rbac002
  10. Nat Protoc. 2022 Apr 27.
      The assay for transposase-accessible chromatin using sequencing (ATAC-seq) provides a simple and scalable way to detect the unique chromatin landscape associated with a cell type and how it may be altered by perturbation or disease. ATAC-seq requires a relatively small number of input cells and does not require a priori knowledge of the epigenetic marks or transcription factors governing the dynamics of the system. Here we describe an updated and optimized protocol for ATAC-seq, called Omni-ATAC, that is applicable across a broad range of cell and tissue types. The ATAC-seq workflow has five main steps: sample preparation, transposition, library preparation, sequencing and data analysis. This protocol details the steps to generate and sequence ATAC-seq libraries, with recommendations for sample preparation and downstream bioinformatic analysis. ATAC-seq libraries for roughly 12 samples can be generated in 10 h by someone familiar with basic molecular biology, and downstream sequencing analysis can be implemented using benchmarked pipelines by someone with basic bioinformatics skills and with access to a high-performance computing environment.
    DOI:  https://doi.org/10.1038/s41596-022-00692-9
  11. Chin J Nat Med. 2022 Apr;pii: S1875-5364(22)60141-9. [Epub ahead of print]20(4): 241-257
      Lysine specific demethylase 1 (LSD1), a transcriptional corepressor or coactivator that serves as a demethylase of histone 3 lysine 4 and 9, has become a potential therapeutic target for cancer therapy. LSD1 mediates many cellular signaling pathways and regulates cancer cell proliferation, invasion, migration, and differentiation. Recent research has focused on the exploration of its pharmacological inhibitors. Natural products are a major source of compounds with abundant scaffold diversity and structural complexity, which have made a major contribution to drug discovery, particularly anticancer agents. In this review, we briefly highlight recent advances in natural LSD1 inhibitors over the past decade. We present a comprehensive review on their discovery and identification process, natural plant sources, chemical structures, anticancer effects, and structure-activity relationships, and finally provide our perspective on the development of novel natural LSD1 inhibitors for cancer therapy.
    Keywords:  Anticancer; Histone lysine demethylase; LSD1 inhibitor; Natural product
    DOI:  https://doi.org/10.1016/S1875-5364(22)60141-9
  12. Technol Cancer Res Treat. 2022 Jan-Dec;21:21 15330338221095950
      Conventional small-molecule drugs (SMDs) are compounds characterized by low molecular weight, high cell permeability, and high selectivity. In clinical translation, SMDs are regarded as good candidates for oral drug formulation. SMD inhibitors play an important role in cancer treatment; however, resistance and low effectiveness have been major bottlenecks in clinical application. Generally, only 20% of cell proteins can potentially be targeted and have been developed as SMDs; thus, some types of tumor targets are considered "undruggable." Among these are transcription factors (TFs), an important class of proteins that regulate the occurrence, formation, and development of tumors. It is difficult for SMDs and macromolecular drugs to identify bioactive sites in TFs and hence for use as pharmacological inhibitors in targeting TF proteins. For this reason, technologies that enable targeted protein degradation, such as proteolysis-targeting chimera or molecular glues, could serve as a potential tool to solve these conundrums.
    Keywords:  PROTAC; molecular glue; protein of interest; targeted protein degradation; transcription factors
    DOI:  https://doi.org/10.1177/15330338221095950