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Cancers
Special Issues
Chromatin-Remodeling Factors in Cancer Cells
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Chromatin-Remodeling Factors in Cancer Cells

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 467

Special Issue Editor

Dr. Sudhakar Jha

E-Mail Website
Guest Editor
Department of Physiological Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater, OK 74078, USA
Interests: epigenetics; chromatin biology; virus-induced cancer; transcription
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chromatin-remodeling and transcription factors are key regulators of the gene expression programs that govern cancer initiation, progression, and response to therapy. Their dysregulation alters chromatin architecture, reprograms cellular states, and creates vulnerabilities that can be therapeutically exploited. As our tools for interrogating the cancer epigenome evolve, new opportunities are emerging for targeting these pathways with precision.

This Special Issue invites original research, reviews, and perspectives exploring the roles of chromatin remodelers and transcription factors in cancer biology and treatment. We welcome studies employing advanced methodologies such as CRISPR-based functional screens, single-cell epigenomics, chromatin conformation capture (e.g., Hi-C), ATAC-seq, and integrative multiomics. Submissions highlighting therapeutic strategies, ranging from small molecule inhibitors and PROTACs to epigenetic drugs and combination therapies, are strongly encouraged.

Topics of interest include mechanistic insights into chromatin dynamics, transcriptional reprogramming in drug resistance, enhancer hijacking, synthetic lethality involving epigenetic regulators, and novel therapeutic platforms targeting chromatin accessibility and transcription factor networks.

Through this Special Issue, we will showcase cutting-edge research that advances our understanding of epigenetic and transcriptional control in cancer, aiming to inform next-generation therapeutic strategies.

Dr. Sudhakar Jha
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chromatin remodeling
  • transcription factors
  • epigenetic therapy
  • cancer epigenomics
  • SWI/SNF complex
  • CRISPR functional screens
  • single-cell epigenomics
  • gene regulation in cancer
  • therapy resistance
  • targeted cancer therapies

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Published Papers (1 paper)

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Research

22 pages, 3032 KiB  
Article
MYC Regulates a DNA Repair Gene Expression Program in Small Cell Carcinoma of the Ovary, Hypercalcemic Type
by James R. Evans, Jing Wang, Cinthia N. Reed, Joy H. Creighton, Kaylee B. Garrison, Abigail N. Robertson, Ashley Lira-Rivera, Diondre’ D. Baisden, William P. Tansey, Rafet Al-Tobasei, Jessica D. Lang, Qi Liu and April M. Weissmiller
Cancers 2025, 17(13), 2255; https://doi.org/10.3390/cancers17132255 - 7 Jul 2025
Viewed by 358
Abstract
Background/Objectives: SCCOHT is an aggressive and often fatal cancer that belongs to the ~20% of cancers defined by mutations to subunits of the SWI/SNF chromatin remodeling complex. In SCCOHT, mutations to the SMARCA4 gene, which encodes the SWI/SNF ATPase BRG1, are sufficient to [...] Read more.
Background/Objectives: SCCOHT is an aggressive and often fatal cancer that belongs to the ~20% of cancers defined by mutations to subunits of the SWI/SNF chromatin remodeling complex. In SCCOHT, mutations to the SMARCA4 gene, which encodes the SWI/SNF ATPase BRG1, are sufficient to impair SWI/SNF function. This single genetic lesion leads to a cascade of events that promote tumorigenesis, some of which may involve the intersection of SWI/SNF with oncogenic pathways such as those regulated by the MYC oncogene. In SCCOHT tumors and other cancers marked by SWI/SNF subunit mutation, MYC target genes are recurrently activated, pointing to a relationship between SWI/SNF and MYC that has yet to be fully explored. Methods: In this study, we investigate the contribution of MYC to SCCOHT biology by performing a combination of chromatin binding and transcriptome assays in genetically engineered SCCOHT cell lines, with subsequent validation using patient tumor expression data. Results: We find that MYC binds to thousands of active promoters in the BIN-67 SCCOHT cell line and that the depletion of MYC results in a broad range of gene expression changes with a notable effect on the expression of genes related to DNA repair. We uncover an MYC-regulated DNA repair gene expression program in BIN-67 cells that is antagonized by BRG1 reintroduction. Finally, we identify a DNA repair gene signature that is upregulated in SCCOHT tumors and in tumors defined by loss of the SWI/SNF subunit SNF5. Conclusions: Collectively, these data implicate MYC as a robust regulator of DNA repair gene expression in SCCOHT and lay a foundation for future studies focused on interrogating the relationship between BRG1 and MYC. Full article
(This article belongs to the Special Issue Chromatin-Remodeling Factors in Cancer Cells)
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