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Molecular Mechanisms of Transcriptional Regulation in Tumor Cell
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Molecular Mechanisms of Transcriptional Regulation in Tumor Cell

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 7433

Special Issue Editors

Prof. Dr. Xiaodong Zhao

E-Mail Website
Guest Editor
Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiaotong University, Shanghai 200240, China
Interests: transcription regulation; epigenetic regulation; polyadenynation and its implication in cancer biology; stem cell biology
Prof. Dr. Yuriy L. Orlov

E-Mail Website
Guest Editor
The Digital Health Institute, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), 119991 Moscow, Russia
Interests: computer genomics; bioinformatics; digital medicine (e-Health); gene expression regulation; ChIP-seq
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The gene expression programs that specify cellular states in humans are regulated by transcription factors, cofactors, and chromatin modifiers. Through binding the cis-regulatory genomic DNA elements and modulating chromatin structure, these transcription regulators recruit and coordinate transcriptional apparatus to control selective gene expression. Dysregulation of these transcription programs can cause the formation and progression of tumor.

An increasing number of studies have revealed that genomic mutations in cis-regulatory regions, transcription factors, cofactors, and chromatin remodeling proteins in tumor cells contribute to abnormal transcription programs, highlighting the link between dysregulation of gene expression and tumor. In addition to these well-recognized transcription regulators, alternative splicing, alternative polyadenylation, non-coding RNA (ncRNA), and RNA-binding proteins have been found to be involved in tumorigenesis due to the rapid development of high-throughput sequencing technology. Such knowledge is improving our understanding of the molecular mechanisms of tumor initiation and progression, which benefits the finding of new approaches to tumor diagnosis and clinical intervention. We welcome the submission of original research articles, brief reports, reviews, and mini reviews about transcription regulation in tumor cells.

Prof. Dr. Xiaodong Zhao
Prof. Dr. Yuriy L. Orlov
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. Genes is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

  • transcription regulation
  • epigenetic regulation
  • tumorigenesis
  • high-throughput sequencing
  • chromatin immunoprecipitation
  • signaling pathway

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Published Papers (2 papers)

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13 pages, 1448 KiB  
Article
The Methylation of the p53 Targets the Genes MIR-203, MIR-129-2, MIR-34A and MIR-34B/C in the Tumor Tissue of Diffuse Large B-Cell Lymphoma
by Elena N. Voropaeva, Tatjana I. Pospelova, Yuriy L. Orlov, Maria I. Churkina, Olga V. Berezina, Anna A. Gurazheva, Tatjana A. Ageeva, Olga B. Seregina and Vladimir N. Maksimov
Genes 2022, 13(8), 1401; https://doi.org/10.3390/genes13081401 - 7 Aug 2022
Cited by 6 | Viewed by 2074
Abstract
The regulation of oncogenes by microRNA is a focus of medical research. hsa-miR-203, hsa-mir-129, hsa-miR-34a, hsa-miR-34b and hsa-miR-34c are oncosuppressive microRNAs that mediate the antitumor activity of p53. We seek to evaluate the frequencies, co-occurrence and clinical significance of the methylation of the [...] Read more.
The regulation of oncogenes by microRNA is a focus of medical research. hsa-miR-203, hsa-mir-129, hsa-miR-34a, hsa-miR-34b and hsa-miR-34c are oncosuppressive microRNAs that mediate the antitumor activity of p53. We seek to evaluate the frequencies, co-occurrence and clinical significance of the methylation of the MIR-203, MIR-129-2, MIR-34A and MIR-34B/C genes in the tumor tissue of diffuse large B-cell lymphoma (DLBCL). The methylation was assessed in 73 samples of DLBCL and in 11 samples of lymph nodes of reactive follicular hyperplasia by Methyl-Specific Polymerase Chain Reaction (MS-PCR) and Methylation-Sensitive High-Resolution-Melting (MS-HRM) methods. All four studied genes were not methylated in the tissue of reactive lymphatic nodes. The methylation frequencies of the MIR-129-2, MIR-203, MIR-34A and MIR-34B/C genes in lymphoma tissue were 67%, 66%, 27% and 62%, respectively. Co-occurrence of MIR-203, MIR-129-2 and MIR-34B/C genes methylation, as well as the methylation of MIR-34B/C and MIR-34A pair genes were detected. The MIR-34A gene methylation was associated with increased International Prognostic Index (IPI) (p = 0.002), whereas the MIR-34B/C (p = 0.026) and MIR-203 (p = 0.011) genes’ methylation was connected with Ki-67 expression level in tumor tissue at more than 45%. We found an increasing frequency of detection of MIR-34A gene methylation in the group of patients with the Germinal-Center B-cell like (GCB-like) subtype of DLBCL (p = 0.046). There was a trend towards a decrease in the remission frequency after the first line of therapy (p = 0.060) and deterioration in overall survival (OS) (p = 0.162) in patients with DLBCL with methylation of the MIR-34A promoter. The methylation of the MIR-34A, MIR-34B/C, MIR-129-2 and MIR-203 genes in DLBCL is tumor-specific and occurs in combination. The methylation of the studied genes may be a potential differential diagnostic biomarker to distinguish between lymphoma and reactive lymph nodes, while its independent predictive value has not been confirmed yet. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Transcriptional Regulation in Tumor Cell)
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21 pages, 3888 KiB  
Article
HNF1A POU Domain Mutations Found in Japanese Liver Cancer Patients Cause Downregulation of HNF4A Promoter Activity with Possible Disruption in Transcription Networks
by Effi Haque, Aamir Salam Teeli, Dawid Winiarczyk, Masahiko Taguchi, Shun Sakuraba, Hidetoshi Kono, Paweł Leszczyński, Mariusz Pierzchała and Hiroaki Taniguchi
Genes 2022, 13(3), 413; https://doi.org/10.3390/genes13030413 - 24 Feb 2022
Cited by 4 | Viewed by 4483
Abstract
Hepatocyte nuclear factor 1A (HNF1A) is the master regulator of liver homeostasis and organogenesis and regulates many aspects of hepatocyte functions. It acts as a tumor suppressor in the liver, evidenced by the increased proliferation in HNF1A knockout (KO) hepatocytes. Hence, we postulated [...] Read more.
Hepatocyte nuclear factor 1A (HNF1A) is the master regulator of liver homeostasis and organogenesis and regulates many aspects of hepatocyte functions. It acts as a tumor suppressor in the liver, evidenced by the increased proliferation in HNF1A knockout (KO) hepatocytes. Hence, we postulated that any loss-of-function variation in the gene structure or composition (mutation) could trigger dysfunction, including disrupted transcriptional networks in liver cells. From the International Cancer Genome Consortium (ICGC) database of cancer genomes, we identified several HNF1A mutations located in the functional Pit-Oct-Unc (POU) domain. In our biochemical analysis, we found that the HNF1A POU-domain mutations Y122C, R229Q and V259F suppressed HNF4A promoter activity and disrupted the binding of HNF1A to its target HNF4A promoter without any effect on the nuclear localization. Our results suggest that the decreased transcriptional activity of HNF1A mutants is due to impaired DNA binding. Through structural simulation analysis, we found that a V259F mutation was likely to affect DNA interaction by inducing large conformational changes in the N-terminal region of HNF1A. The results suggest that POU-domain mutations of HNF1A downregulate HNF4A gene expression. Therefore, to mimic the HNF1A mutation phenotype in transcription networks, we performed siRNA-mediated knockdown (KD) of HNF4A. Through RNA-Seq data analysis for the HNF4A KD, we found 748 differentially expressed genes (DEGs), of which 311 genes were downregulated (e.g., HNF1A, ApoB and SOAT2) and 437 genes were upregulated. Kyoto Encyclopedia of Genes and Genomes (KEGG) mapping revealed that the DEGs were involved in several signaling pathways (e.g., lipid and cholesterol metabolic pathways). Protein–protein network analysis suggested that the downregulated genes were related to lipid and cholesterol metabolism pathways, which are implicated in hepatocellular carcinoma (HCC) development. Our study demonstrates that mutations of HNF1A in the POU domain result in the downregulation of HNF1A target genes, including HNF4A, and this may trigger HCC development through the disruption of HNF4A–HNF1A transcriptional networks. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Transcriptional Regulation in Tumor Cell)
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