Special lssues
Table of Content

Epigenetic Regulation of Cancer

Submission Deadline: 31 October 2023 (closed)

Guest Editors


Dr. Ajay Kumar Singh
Department of Bioinformatics, Central University of South Bihar, India
Email: ajaysingh@cusb.ac.in, ajjay2@gmail.com


Dr. Taicheng Zhou
Department of Gastroenterological Surgery and Hernia Center, The Sixth Affiliated Hospital, Sun Yat-sen University, China
Email: zhoutaicheng@126.com, zhoutch3@mail.sysu.edu.cn (Preferred)

Coordinator

Enmin Huang
Department of Gastroenterological Surgery and Hernia Center, The Sixth Affiliated Hospital, Sun Yat-sen University, China
Email: huangenm5@mail.sysu.edu.cn

Summary

Epigenetics can be defined as changes of heritable nature in the gene expression but the DNA sequence remains unchanged. This phenomenon affects the nature of cells reading the genes. In current scenario, owing to the technological advancements in the field of genetics, a plethora of diseases are being found to have epigenetic implications. Among these diseases, the implication of epigenetic regulations in cancer stands out from the rest. The cancer disease being linked with epigenetic regulation opens the door for gaining an understanding of the genes involved with the disease and whether those genes can be manipulated to control the production or barring the production of certain proteins or enzymes in specific cells, which might end up proving beneficial in the course of tackling a disease of the magnitude of cancer. It is important to understand that epigenetics cannot be explained with a single definition, since the word has numerous meanings belonging to different sources. Therefore it is accurate to consider epigenetics as an umbrella term, to include any mechanism which causes a change in the genetic activity but keeps the DNA sequence unchanged. A variety of epigenetic mechanisms have been identified throughout the years and more processes are on the verge of being identified. It is important to devote our attention in understanding these mechanisms, since engineering these may help us modify and control specific genes in their expression. This also holds true in the case of cancer treatment and prevention. Manipulation of epigenetic alterations holds great promise for cancer prevention, detection, and therapy, which might lead to a probable cure or better understanding of the disease. It is a known fact nowadays that cancer is a genetic disease. The driving force behind it being alteration of the oncogenic genes and tumor suppressors. Epigenetic alterations behind the cause of cancer are speculated to be DNA methylation, acetylation, or phosphorylation of histones and other proteins around which DNA is wound to form chromatin.

 

The proposed topic welcome the content related to epigenetic various issues of cancer which mainly includes the cancer mechanism, marker development, Insilico interaction analysis, Drug designing, Cancer treatment therapies, cancer recurrence mechanism and treatment.

 

More issue details:

-The development of new epigenetic agents and combinations of immunotherapies and epigenetic therapies.

-Application of DNA methyltransferase (DNMT) and histone deacetylase (HDAC) regulators.

-The role of non-coding RNAs (including circular RNAs, lncRNAs, miRNAs, etc.) in the epigenetic regulation of cancer.

-Identification of epigenetic and metabolic immune markers associated with cancer outcomes, including occurrence and progression.

-Single-cell epigenome and transcriptome analysis and other approaches to map cellular networks driving susceptibility to cancer.

-Epigenetic profiling of rare immune cell populations in cancer patients.


Keywords

epigenetic, immune, non-coding RNAs, metabolic, single-cell epigenome

Published Papers


  • Open Access

    ARTICLE

    UCHL5 inhibits U251 glioma cell proliferation and tumor growth via stabilizing and deubiquitinating PTEN

    YUE XIAO, WENJING MA, XINYI CHEN, WEIWEI HU, QIANQIAN DI, XIBAO ZHAO, GUODONG HUANG, WEILIN CHEN
    BIOCELL, Vol.47, No.12, pp. 2617-2625, 2023, DOI:10.32604/biocell.2023.042476
    (This article belongs to this Special Issue: Epigenetic Regulation of Cancer)
    Abstract Background: Glioma is the most common primary brain tumor. Exploration of new tumorigenesis mechanism of glioma is critical to determine more effective treatment targets as well as to develop effective prognosis methods that can enhance the treatment efficacy. We previously demonstrated that the deubiquitinase biquitin carboxyl-terminal hydrolase L5 (UCHL5) was downregulated in human glioma. However, the effect and mechanism of UCHL5 on the proliferation of glioma cells remains unknown. Methods: Transfection of siRNA was used to knockdown the expression of UCHL5 in U251 cells. The 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, Edu assay, and colony formation assay were employed to… More >

    Graphic Abstract

    UCHL5 inhibits U251 glioma cell proliferation and tumor growth via stabilizing and deubiquitinating PTEN

Share Link