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Cells
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Transcription and Chromatin Dysregulation in Cancer
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Transcription and Chromatin Dysregulation in Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell and Gene Therapy".

Deadline for manuscript submissions: closed (20 June 2023) | Viewed by 10655

Special Issue Editors

Dr. Yinghui Li

E-Mail Website
Guest Editor
School of Biological Sciences (SBS), Nanyang Technological University (NTU), 60 Nanyang Drive, Singapore 637551, Singapore
Interests: cancer epigenomics; RNA biology; cancer cell signaling; gene regulation
Dr. Kamalakshi Deka

E-Mail Website
Guest Editor
School of Biological Sciences (SBS), Nanyang Technological University (NTU), 60 Nanyang Drive, Singapore 637551, Singapore
Interests: cancer genetics; epigenetics; RNA biology; RNA–protein interaction; RNA therapeutics; post-translational modification; non-coding RNAs; stress biology

Special Issue Information

Dear Colleagues,

Cellular homeostasis relies on the programmed transcriptional machinery in a cell. Any disruption in the process of transcriptional control in turn causes aberrant gene expression that underscores the main hallmarks of cancer cells. Generally, the molecular regulators of these programmed signaling cascades involve transcription factors (TFs), which are being extensively studied to be targeted by various anti-tumor therapeutic approaches. However, recent advances in sequencing the data of cancer genomes have unveiled several changes occurring at the level of chromatin structure and epigenetics, affecting other components of the transcriptional control involving cis and trans regulatory elements and chromatin modifiers. Hence, it is of the utmost importance to understand how chromatin modifiers integrate both extracellular and cytoplasmic signals to control gene activity. Most common dysregulation occurring at the level of chromatin remodelers leading to oncogenesis involves inactivating mutations in SWI/SNF complex, epigenetic silencing via DNA and histone hypermethylation, and overexpression of oncogenic chromatin modifiers (Mi-2/NuRD proteins). In addition, the pattern of histone modification also controls the tumorigenic nature of cells depending on interaction between TFs and histone modifiers. One such modification involves the monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation at lysine 27 (H3K27ac), leading to the activation of a long stretch of oncogenic enhancers called super-enhancers (SEs).

The aim of this Special Issue is to explore and provide our readers with more insight into the oncogenic signal(s) and regulatory mechanisms at the level of chromatin that drive cancer development and progression. We invite original communications and review articles which can help us to understand the complex nature of epigenetic regulation that transforms the canonical role of TFs to become oncogenic, and how the interaction dynamics between chromatin modifiers, histone marks and cis/trans regulatory elements controls the entire tumorigenic landscape, with a view to identifying probable new cancer biomarkers and strategies for targeting them as means of therapeutic intervention.

Dr. Yinghui Li
Dr. Kamalakshi Deka
Guest Editors

Manuscript Submission Information

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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. Cells 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 2700 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

  • transcriptional regulation
  • chromatin modifiers
  • chromatin dysregulation
  • epigenetics
  • epigenomics
  • chromatin interaction
  • super-enhancers
  • histone modification
  • oncogene
  • cancer cell signaling
  • cancer

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Published Papers (3 papers)

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Research

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22 pages, 4223 KiB  
Article
Differential Occupancy and Regulatory Interactions of KDM6A in Bladder Cell Lines
by Gülden Özden-Yılmaz, Busra Savas, Ahmet Bursalı, Aleyna Eray, Alirıza Arıbaş, Serif Senturk, Ezgi Karaca, Gökhan Karakülah and Serap Erkek-Ozhan
Cells 2023, 12(6), 836; https://doi.org/10.3390/cells12060836 - 8 Mar 2023
Cited by 1 | Viewed by 2570
Abstract
Epigenetic deregulation is a critical theme which needs further investigation in bladder cancer research. One of the most highly mutated genes in bladder cancer is KDM6A, which functions as an H3K27 demethylase and is one of the MLL3/4 complexes. To decipher the [...] Read more.
Epigenetic deregulation is a critical theme which needs further investigation in bladder cancer research. One of the most highly mutated genes in bladder cancer is KDM6A, which functions as an H3K27 demethylase and is one of the MLL3/4 complexes. To decipher the role of KDM6A in normal versus tumor settings, we identified the genomic landscape of KDM6A in normal, immortalized, and cancerous bladder cells. Our results showed differential KDM6A occupancy in the genes involved in cell differentiation, chromatin organization, and Notch signaling depending on the cell type and the mutation status of KDM6A. Transcription factor motif analysis revealed HES1 to be enriched at KDM6A peaks identified in the T24 bladder cancer cell line; moreover, it has a truncating mutation in KDM6A and lacks a demethylase domain. Our co-immunoprecipitation experiments revealed TLE co-repressors and HES1 as potential truncated and wild-type KDM6A interactors. With the aid of structural modeling, we explored how truncated KDM6A could interact with TLE and HES1, as well as RUNX and HHEX transcription factors. These structures provide a solid means of studying the functions of KDM6A independently of its demethylase activity. Collectively, our work provides important contributions to the understanding of KDM6A malfunction in bladder cancer. Full article
(This article belongs to the Special Issue Transcription and Chromatin Dysregulation in Cancer)
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Review

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24 pages, 1210 KiB  
Review
Transcriptional Regulation during Aberrant Activation of NF-κB Signalling in Cancer
by Kamalakshi Deka and Yinghui Li
Cells 2023, 12(5), 788; https://doi.org/10.3390/cells12050788 - 2 Mar 2023
Cited by 27 | Viewed by 3588
Abstract
The NF-κB signalling pathway is a major signalling cascade involved in the regulation of inflammation and innate immunity. It is also increasingly recognised as a crucial player in many steps of cancer initiation and progression. The five members of the NF-κB family of [...] Read more.
The NF-κB signalling pathway is a major signalling cascade involved in the regulation of inflammation and innate immunity. It is also increasingly recognised as a crucial player in many steps of cancer initiation and progression. The five members of the NF-κB family of transcription factors are activated through two major signalling pathways, the canonical and non-canonical pathways. The canonical NF-κB pathway is prevalently activated in various human malignancies as well as inflammation-related disease conditions. Meanwhile, the significance of non-canonical NF-κB pathway in disease pathogenesis is also increasingly recognized in recent studies. In this review, we discuss the double-edged role of the NF-κB pathway in inflammation and cancer, which depends on the severity and extent of the inflammatory response. We also discuss the intrinsic factors, including selected driver mutations, and extrinsic factors, such as tumour microenvironment and epigenetic modifiers, driving aberrant activation of NF-κB in multiple cancer types. We further provide insights into the importance of the interaction of NF-κB pathway components with various macromolecules to its role in transcriptional regulation in cancer. Finally, we provide a perspective on the potential role of aberrant NF-κB activation in altering the chromatin landscape to support oncogenic development. Full article
(This article belongs to the Special Issue Transcription and Chromatin Dysregulation in Cancer)
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22 pages, 3065 KiB  
Review
Pathological Role of HDAC8: Cancer and Beyond
by Ji Yoon Kim, Hayoung Cho, Jung Yoo, Go Woon Kim, Yu Hyun Jeon, Sang Wu Lee and So Hee Kwon
Cells 2022, 11(19), 3161; https://doi.org/10.3390/cells11193161 - 9 Oct 2022
Cited by 38 | Viewed by 3948
Abstract
Histone deacetylase 8 (HDAC8) is a class I HDAC that catalyzes the deacetylation of histone and non-histone proteins. As one of the best-characterized isoforms, numerous studies have identified interacting partners of HDAC8 pertaining to diverse molecular mechanisms. Consequently, deregulation and overexpression of HDAC8 [...] Read more.
Histone deacetylase 8 (HDAC8) is a class I HDAC that catalyzes the deacetylation of histone and non-histone proteins. As one of the best-characterized isoforms, numerous studies have identified interacting partners of HDAC8 pertaining to diverse molecular mechanisms. Consequently, deregulation and overexpression of HDAC8 give rise to diseases. HDAC8 is especially involved in various aspects of cancer progression, such as cancer cell proliferation, metastasis, immune evasion, and drug resistance. HDAC8 is also associated with the development of non-cancer diseases such as Cornelia de Lange Syndrome (CdLS), infectious diseases, cardiovascular diseases, pulmonary diseases, and myopathy. Therefore, HDAC8 is an attractive therapeutic target and various HDAC8 selective inhibitors (HDAC8is) have been developed. Here, we address the pathological function of HDAC8 in cancer and other diseases, as well as illustrate several HDAC8is that have shown anti-cancer effects. Full article
(This article belongs to the Special Issue Transcription and Chromatin Dysregulation in Cancer)
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