Yeast Bromodomain Factor 1 and Its Human Homolog TAF1 Play Conserved Roles in Promoting Homologous Recombination

Peng, Haoyang; Zhang, Simin; Peng, Yangqin; Zhu, Shuangyi; Zhao, Xin; Zhao, Xiaocong; Yang, Shuangshuang; Liu, Guang-Xue; Dong, Yan; Gan, Xiaoli; Li, Qing; Zhang, Xinghua; Pei, Huadong; Chen, Xuefeng

doi:10.1002/advs.202100753

Cited by 11 publications

(6 citation statements)

References 77 publications

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“…Chromatin Immunoprecipitation (ChIP) assays were performed essentially as described before ( Coarfa et al, 2020 ; Hu et al, 2020 ; Jehanno et al, 2020 ; Maity et al, 2020 ; Mallik et al, 2020 ; Moon et al, 2020 ; Shen et al, 2020 ; Wang J. N. et al, 2020 ; Wang S. et al, 2020 ; Zhang et al, 2020 ; Zhao et al, 2020 ; Marti et al, 2021 ; Peng et al, 2021 ; Rashid et al, 2021 ). In brief, chromatin in control and treated cells were cross-linked with 1% formaldehyde.…”

Section: Methodsmentioning

confidence: 99%

A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells

Chen

Dong

Shao

et al. 2021

Front. Cell Dev. Biol.

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Intestinal fibrosis is one of the common pathophysiological processes in inflammatory bowel diseases (IBDs). Previously it has been demonstrated that epithelial-mesenchymal transition (EMT) can contribute to the development of intestinal fibrosis. Here we report that conditional ablation of SIRT1, a class III lysine deacetylase, in intestinal epithelial cells exacerbated 2, 4, 6-trinitro-benzene sulfonic acid (TNBS) induced intestinal fibrosis in mice. SIRT1 activity, but not SIRT1 expression, was down-regulated during EMT likely due to up-regulation of its inhibitor deleted in breast cancer 1 (DBC1). TGF-β augmented the recruitment of KDM4A, a histone H3K9 demethylase, to the DBC1 promoter in cultured intestinal epithelial cells (IEC-6) leading to DBC1 trans-activation. KDM4A depletion or inhibition abrogated DBC1 induction by TGF-β and normalized SIRT1 activity. In addition, KDM4A deficiency attenuated TGF-β induced EMT in IEC-6 cells. In conclusion, our data identify a KDM4-DBC1-SIRT1 pathway that regulates EMT to contribute to intestinal fibrosis.

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Section: Methodsmentioning

confidence: 99%

A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells

Chen

Dong

Shao

et al. 2021

Front. Cell Dev. Biol.

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“…Furthermore, in glioblastoma xenografts, OTX015 showed additive to synergistic efficacy when paired with irinotecan [ 106 ]. The depletion or disruption of yeast Bromodomain Factor 1 or Bromodomain Factor 2 (its human counterpart TAF1) was found to increase susceptibility to CPT through inhibiting the DNA end resection and repair [ 107 , 108 ].…”

Section: Epigenetic Modifications and The Response Of Cancer Cells To...mentioning

confidence: 99%

Epigenetic modulations in cancer: predictive biomarkers and potential targets for overcoming the resistance to topoisomerase I inhibitors

et al. 2023

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Introduction Altered epigenetic map is frequently observed in cancer and recent investigations have demonstrated a pertinent role of epigenetic modifications in the response to many anticancer drugs including the DNA damaging agents. Topoisomerase I (Top I) is a well-known nuclear enzyme that is critical for DNA function and cell survival and its inhibition causes DNA strand breaks and cell cycle arrest. Inhibitors of human Top I have proven to be a prosperous chemotherapeutic treatment for a vast number of cancer patients. While the treatment is efficacious in many cases, resistance and altered cellular response remain major therapeutic issues. Areas covered This review highlights the evidence available till date on the influence of different epigenetic modifications on the response to Top I inhibitors as well as the implications of targeting epigenetic alterations for improving the efficacy and safety of Top I inhibitors. Expert opinion The field of epigenetic research is steadily growing. With its assistance, we could gain better understanding on how drug response and resistance work. Epigenetics can evolve as possible biomarkers and predictors of response to many medications including Top I inhibitors, and could have significant clinical implications that necessitate deeper attention. HIGHLIGHTS Epigenetic alterations, including DNA methylation and histone modifications, play a pertinent role in the response to several anticancer treatments, including DNA damaging agents like Top I inhibitors. Although camptothecin derivatives are used clinically as Top I inhibitors for management of cancer, certain types of cancer have inherent and or acquired resistance that limit the curative potential of them. Epigenetic modifications like DNA hypomethylation can either increase or decrease sensitivity to Top I inhibitors by different mechanisms. The combination of Top I inhibitors with the inhibitors of histone modifying enzymes can result in enhanced cytotoxic effects and sensitization of resistant cells to Top I inhibitors. MicroRNAs were found to directly influence the expression of Top I and other proteins in cancer cells resulting in positive or negative alteration of the response to Top I inhibitors. lncRNAs and their genetic polymorphisms have been found to be associated with Top I function and the response to its inhibitors. Clinical trials of epigenetic drugs in combination with Top I inhibitors are plentiful and some of them showed potentially promising outcomes.

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“…Chromatin immunoprecipitation (ChIP) assays were performed essentially as described before (Coarfa et al, 2020;Hu et al, 2020;Jehanno et al, 2020;Maity et al, 2020;Mallik et al, 2020;Moon et al, 2020;Shen et al, 2020;Wang et al, 2020a,b;Zhang et al, 2020;Zhao et al, 2020;Marti et al, 2021;Peng et al, 2021;Rashid et al, 2021). In brief, chromatin in control and treated cells were cross-linked with 1% formaldehyde.…”

Section: Chromatin Immunoprecipitationmentioning

confidence: 99%

Choline Kinase Alpha Is a Novel Transcriptional Target of the Brg1 in Hepatocyte: Implication in Liver Regeneration

Kong

Dong

et al. 2021

Front. Cell Dev. Biol.

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Liver regeneration is a key compensatory process in response to liver injury serving to contain damages and to rescue liver functions. Hepatocytes, having temporarily exited the cell cycle after embryogenesis, resume proliferation to regenerate the injured liver parenchyma. In the present study we investigated the transcriptional regulation of choline kinase alpha (Chka) in hepatocytes in the context of liver regeneration. We report that Chka expression was significantly up-regulated in the regenerating livers in the partial hepatectomy (PHx) model and the acetaminophen (APAP) injection model. In addition, treatment with hepatocyte growth factor (HGF), a strong pro-proliferative cue, stimulated Chka expression in primary hepatocytes. Chka depletion attenuated HGF-induced proliferation of hepatocytes as evidenced by quantitative PCR and Western blotting measurements of pro-proliferative genes as well as EdU incorporation into replicating DNA. Of interest, deletion of Brahma-related gene 1 (Brg1), a chromatin remodeling protein, attenuated Chka induction in the regenerating livers in mice and in cultured hepatocytes. Further analysis revealed that Brg1 interacted with hypoxia-inducible factor 1 alpha (HIF-1α) to directly bind to the Chka promoter and activate Chka transcription. Finally, examination of human acute liver failure (ALF) specimens identified a positive correlation between Chka expression and Brg1 expression. In conclusion, our data suggest that Brg1-dependent trans-activation of Chka expression may contribute to liver regeneration.

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Yeast Bromodomain Factor 1 and Its Human Homolog TAF1 Play Conserved Roles in Promoting Homologous Recombination

Cited by 11 publications

References 77 publications

A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells

A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells

Epigenetic modulations in cancer: predictive biomarkers and potential targets for overcoming the resistance to topoisomerase I inhibitors

Choline Kinase Alpha Is a Novel Transcriptional Target of the Brg1 in Hepatocyte: Implication in Liver Regeneration

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