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Cancers
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Phase Separation, Chromatin Organization and Transcription for Cancers
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Phase Separation, Chromatin Organization and Transcription for Cancers

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

Deadline for manuscript submissions: closed (1 September 2022) | Viewed by 23413

Special Issue Editors

Prof. Dr. Reshma Taneja

E-Mail Website
Guest Editor
Head, Deparment of Physiology, NUS Yong Loo Lin School of Medicine, Singapore City, Singapore
Interests: cancer; epigenetics; transcription; gene regulation; myogenesis; differentiation
Dr. Sudhakar Jha

E-Mail Website
Guest Editor
Cancer Science Institute of National University of Singapore, 117599 Singapore City, Singapore
Interests: epigenetics; chromatin biology; virus-induced cancer; transcription

Special Issue Information

Dear Colleagues,

Our genome is organized in the nucleus where DNA is wrapped around histone proteins to form chromatin. Any access to the DNA requires factors that help in chromatin reorganization, such as decompaction and compaction of the chromatin. Many factors influence the maintenance and regulation of these higher-order structures, also known as chromatin domains. Among these, epigenetic regulators play a vital role in remodeling the chromatin landscape to maintain transcriptionally active and repressed domains. In this issue, we will showcase recent discoveries in the field that have identified phase-separation and chromatin domains to be dysregulated in cancers and their influence on gene expression.

Prof. Dr. Reshma Taneja
Dr. Sudhakar Jha
Guest Editors

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

  • transcription
  • chromatin
  • gene regulation
  • histones
  • cancer
  • epigenetics

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Published Papers (5 papers)

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Review

13 pages, 702 KiB  
Review
IRF4 as an Oncogenic Master Transcription Factor
by Regina Wan Ju Wong, Jolynn Zu Lin Ong, Madelaine Skolastika Theardy and Takaomi Sanda
Cancers 2022, 14(17), 4314; https://doi.org/10.3390/cancers14174314 - 2 Sep 2022
Cited by 18 | Viewed by 5663
Abstract
IRF4 is a transcription factor in the interferon regulatory factor (IRF) family. Since the discovery of this gene, various research fields including immunology and oncology have highlighted the unique characteristics and the importance of IRF4 in several biological processes that distinguish it from [...] Read more.
IRF4 is a transcription factor in the interferon regulatory factor (IRF) family. Since the discovery of this gene, various research fields including immunology and oncology have highlighted the unique characteristics and the importance of IRF4 in several biological processes that distinguish it from other IRF family members. In normal lymphocyte development and immunity, IRF4 mediates critical immune responses via interactions with upstream signaling pathways, such as the T-cell receptor and B-cell receptor pathways, as well as their binding partners, which are uniquely expressed in each cell type. On the other hand, IRF4 acts as an oncogene in various mature lymphoid neoplasms when abnormally expressed. IRF4 induces several oncogenes, such as MYC, as well as genes that characterize each cell type by utilizing its ability as a master regulator of immunity. IRF4 and its upstream factor NF-κB form a transcriptional regulatory circuit, including feedback and feedforward loops, to maintain the oncogenic transcriptional program in malignant lymphoid cells. In this review article, we provide an overview of the molecular functions of IRF4 in mature lymphoid neoplasms and highlight its upstream and downstream pathways, as well as the regulatory circuits mediated by IRF4. Full article
(This article belongs to the Special Issue Phase Separation, Chromatin Organization and Transcription for Cancers)
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18 pages, 1150 KiB  
Review
Cancer Cachexia: Signaling and Transcriptional Regulation of Muscle Catabolic Genes
by Vinay Kumar Rao, Dipanwita Das and Reshma Taneja
Cancers 2022, 14(17), 4258; https://doi.org/10.3390/cancers14174258 - 31 Aug 2022
Cited by 8 | Viewed by 4669
Abstract
Cancer cachexia (CC) is a multifactorial syndrome characterized by a significant reduction in body weight that is predominantly caused by the loss of skeletal muscle and adipose tissue. Although the ill effects of cachexia are well known, the condition has been largely overlooked, [...] Read more.
Cancer cachexia (CC) is a multifactorial syndrome characterized by a significant reduction in body weight that is predominantly caused by the loss of skeletal muscle and adipose tissue. Although the ill effects of cachexia are well known, the condition has been largely overlooked, in part due to its complex etiology, heterogeneity in mediators, and the involvement of diverse signaling pathways. For a long time, inflammatory factors have been the focus when developing therapeutics for the treatment of CC. Despite promising pre-clinical results, they have not yet advanced to the clinic. Developing new therapies requires a comprehensive understanding of how deregulated signaling leads to catabolic gene expression that underlies muscle wasting. Here, we review CC-associated signaling pathways and the transcriptional cascade triggered by inflammatory cytokines. Further, we highlight epigenetic factors involved in the transcription of catabolic genes in muscle wasting. We conclude with reflections on the directions that might pave the way for new therapeutic approaches to treat CC. Full article
(This article belongs to the Special Issue Phase Separation, Chromatin Organization and Transcription for Cancers)
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Figure 1

23 pages, 1110 KiB  
Review
Super-Enhancers, Phase-Separated Condensates, and 3D Genome Organization in Cancer
by Seng Chuan Tang, Udhaya Vijayakumar, Ying Zhang and Melissa Jane Fullwood
Cancers 2022, 14(12), 2866; https://doi.org/10.3390/cancers14122866 - 10 Jun 2022
Cited by 18 | Viewed by 5879
Abstract
3D chromatin organization plays an important role in transcription regulation and gene expression. The 3D genome is highly maintained by several architectural proteins, such as CTCF, Yin Yang 1, and cohesin complex. This structural organization brings regulatory DNA elements in close proximity to [...] Read more.
3D chromatin organization plays an important role in transcription regulation and gene expression. The 3D genome is highly maintained by several architectural proteins, such as CTCF, Yin Yang 1, and cohesin complex. This structural organization brings regulatory DNA elements in close proximity to their target promoters. In this review, we discuss the 3D chromatin organization of super-enhancers and their relationship to phase-separated condensates. Super-enhancers are large clusters of DNA elements. They can physically contact with their target promoters by chromatin looping during transcription. Multiple transcription factors can bind to enhancer and promoter sequences and recruit a complex array of transcriptional co-activators and RNA polymerase II to effect transcriptional activation. Phase-separated condensates of transcription factors and transcriptional co-activators have been implicated in assembling the transcription machinery at particular enhancers. Cancer cells can hijack super-enhancers to drive oncogenic transcription to promote cell survival and proliferation. These dysregulated transcriptional programs can cause cancer cells to become highly dependent on transcriptional regulators, such as Mediator and BRD4. Moreover, the expression of oncogenes that are driven by super-enhancers is sensitive to transcriptional perturbation and often occurs in phase-separated condensates, supporting therapeutic rationales of targeting SE components, 3D genome organization, or dysregulated condensates in cancer. Full article
(This article belongs to the Special Issue Phase Separation, Chromatin Organization and Transcription for Cancers)
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26 pages, 1286 KiB  
Review
Potential Therapeutics Targeting Upstream Regulators and Interactors of EHMT1/2
by Gareth Chin Khye Ang, Amogh Gupta, Shirlyn Xue Ling Yap, Uttam Surana and Reshma Taneja
Cancers 2022, 14(12), 2855; https://doi.org/10.3390/cancers14122855 - 9 Jun 2022
Cited by 1 | Viewed by 3183
Abstract
Euchromatin histone lysine methyltransferases (EHMTs) are epigenetic regulators responsible for silencing gene transcription by catalyzing H3K9 dimethylation. Dysregulation of EHMT1/2 has been reported in multiple cancers and is associated with poor clinical outcomes. Although substantial insights have been gleaned into the downstream targets [...] Read more.
Euchromatin histone lysine methyltransferases (EHMTs) are epigenetic regulators responsible for silencing gene transcription by catalyzing H3K9 dimethylation. Dysregulation of EHMT1/2 has been reported in multiple cancers and is associated with poor clinical outcomes. Although substantial insights have been gleaned into the downstream targets and pathways regulated by EHMT1/2, few studies have uncovered mechanisms responsible for their dysregulated expression. Moreover, EHMT1/2 interacting partners, which can influence their function and, therefore, the expression of target genes, have not been extensively explored. As none of the currently available EHMT inhibitors have made it past clinical trials, understanding upstream regulators and EHMT protein complexes may provide unique insights into novel therapeutic avenues in EHMT-overexpressing cancers. Here, we review our current understanding of the regulators and interacting partners of EHMTs. We also discuss available therapeutic drugs that target the upstream regulators and binding partners of EHMTs and could potentially modulate EHMT function in cancer progression. Full article
(This article belongs to the Special Issue Phase Separation, Chromatin Organization and Transcription for Cancers)
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15 pages, 3957 KiB  
Review
Large-Scale Chromatin Rearrangements in Cancer
by Kosuke Yamaguchi, Xiaoying Chen, Asami Oji, Ichiro Hiratani and Pierre-Antoine Defossez
Cancers 2022, 14(10), 2384; https://doi.org/10.3390/cancers14102384 - 12 May 2022
Cited by 2 | Viewed by 3214
Abstract
Epigenetic abnormalities are extremely widespread in cancer. Some of them are mere consequences of transformation, but some actively contribute to cancer initiation and progression; they provide powerful new biological markers, as well as new targets for therapies. In this review, we examine the [...] Read more.
Epigenetic abnormalities are extremely widespread in cancer. Some of them are mere consequences of transformation, but some actively contribute to cancer initiation and progression; they provide powerful new biological markers, as well as new targets for therapies. In this review, we examine the recent literature and focus on one particular aspect of epigenome deregulation: large-scale chromatin changes, causing global changes of DNA methylation or histone modifications. After a brief overview of the one-dimension (1D) and three-dimension (3D) epigenome in healthy cells and of its homeostasis mechanisms, we use selected examples to describe how many different events (mutations, changes in metabolism, and infections) can cause profound changes to the epigenome and fuel cancer. We then present the consequences for therapies and briefly discuss the role of single-cell approaches for the future progress of the field. Full article
(This article belongs to the Special Issue Phase Separation, Chromatin Organization and Transcription for Cancers)
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