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Genes
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Gene Regulation in Cancers
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Gene Regulation in Cancers

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

Deadline for manuscript submissions: closed (25 February 2023) | Viewed by 10321

Special Issue Editors

Prof. Dr. Xin Liu

E-Mail Website
Guest Editor
Center for Excellence in Molecular Cell Science (Shanghai Institute of Biochemistry and Cell Biology, SIBCB), Chinese Academy of Sciences, Shanghai, China
Interests: epigenetics; chromatin structure; non-coding genome; transcriptional regulation
Prof. Dr. Yihui Fan

E-Mail
Guest Editor
Department of Pathogenic Biology, School of Medicine, Nantong University, Nantong, China
Interests: enhancer; super-enhancer; transcriptional regulation; DNA regulatory elements
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Maintaining cell identity requires a coordinated regulation of gene expression. Gene expression dysregulation, leading to the loss of cell identity, can promote tumorigenesis. Recently, the application of omics-based technologies has increasingly expanded our scope of underlying gene regulatory mechanisms in cancer. Different stages of the gene regulatory programs can be affected by a wide variety of events, including accumulative coding and/or non-coding genetic mutations, DNA/RNA and histone modifications, chromatin conformation changes, and rewired metabolic pathways. An improved systematic understanding of gene regulation will provide profound insights into the mechanisms of tumorigenesis and lead to the development of novel diagnoses and therapies for treating cancer.

This Special Issue of Genes aims to highlight the latest advances in the molecular mechanisms of altered gene expression regulation in cancer onset and progression. We invite authors to submit reviews, original articles, new experimental and computational methods, and commentaries, which focus on any of the following topics: genetic variations influencing the cancer transcriptome, signaling pathways and/or epigenetic modulators aberrantly reprogramming cancer epigenome, cancer-related metabolites impairing epigenetic modifications, mechanisms impacting RNA processing in cancer, and novel therapeutic strategies conquering cancer-specific gene regulation programs. We look forward to your contributions.

Prof. Dr. Xin Liu
Prof. Dr. Yihui Fan
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 short 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. Genes is an international peer-reviewed open access monthly 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 2600 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

  • epigenetics
  • genomics
  • transcriptomics
  • metabolomics
  • multi-omics
  • gene expression
  • cancer
  • transcriptional regulation

Published Papers (5 papers)

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Research

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11 pages, 281 KiB  
Article
An Assessment of MT1A (rs11076161), MT2A (rs28366003) and MT1L (rs10636) Gene Polymorphisms and MT2 Concentration in Women with Endometrial Pathologies
by Kaja Michalczyk, Patrycja Kapczuk, Grzegorz Witczak, Piotr Tousty, Mateusz Bosiacki, Mateusz Kurzawski, Dariusz Chlubek and Aneta Cymbaluk-Płoska
Genes 2023, 14(3), 773; https://doi.org/10.3390/genes14030773 - 22 Mar 2023
Viewed by 1445
Abstract
Several studies have indicated a relationship between metallothionein (MT) polymorphisms and the development of different pathologies, including neoplastic diseases. However, no studies thus far have been conducted on the influence of MT polymorphisms and the development of endometrial lesions, including endometrial cancer. This [...] Read more.
Several studies have indicated a relationship between metallothionein (MT) polymorphisms and the development of different pathologies, including neoplastic diseases. However, no studies thus far have been conducted on the influence of MT polymorphisms and the development of endometrial lesions, including endometrial cancer. This study included 140 patients with normal endometrial tissue, endometrial polyps, uterine myomas and endometrial cancer. The tissue MT2 concentration was determined using the ELISA method. MT1A, MT2A and MT1L polymorphisms were analyzed using TaqMan real-time PCR genotyping assays. We found no statistical difference between the tissue MT2 concentration in patients with EC vs. benign endometrium (p = 0.579). However, tissue MT2 concentration was significantly different between uterine fibromas and normal endometrial tissue samples (p = 0.019). Menopause status did not influence the tissue MT2 concentration (p = 0.282). There were no significant associations between the prevalence of MT1A, MT2A and MT1L polymorphisms and MT2 concentration. The age, menopausal status, and diabetes status of patients were identified as EC risk factors. Full article
(This article belongs to the Special Issue Gene Regulation in Cancers)
15 pages, 4871 KiB  
Article
Single-Cell Sequencing Identifies Master Regulators Affected by Panobinostat in Neuroblastoma Cells
by Giorgio Milazzo, Giovanni Perini and Federico M. Giorgi
Genes 2022, 13(12), 2240; https://doi.org/10.3390/genes13122240 - 29 Nov 2022
Cited by 3 | Viewed by 1966
Abstract
The molecular mechanisms and gene regulatory networks sustaining cell proliferation in neuroblastoma (NBL) cells are still not fully understood. In this tumor context, it has been proposed that anti-proliferative drugs, such as the pan-HDAC inhibitor panobinostat, could be tested to mitigate tumor progression. [...] Read more.
The molecular mechanisms and gene regulatory networks sustaining cell proliferation in neuroblastoma (NBL) cells are still not fully understood. In this tumor context, it has been proposed that anti-proliferative drugs, such as the pan-HDAC inhibitor panobinostat, could be tested to mitigate tumor progression. Here, we set out to investigate the effects of panobinostat treatment at the unprecedented resolution offered by single-cell sequencing. We identified a global senescence signature paired with reduction in proliferation in treated Kelly cells and more isolated transcriptional responses compatible with early neuronal differentiation. Using master regulator analysis, we identified BAZ1A, HCFC1, MAZ, and ZNF146 as the transcriptional regulators most significantly repressed by panobinostat. Experimental silencing of these transcription factors (TFs) confirmed their role in sustaining NBL cell proliferation in vitro. Full article
(This article belongs to the Special Issue Gene Regulation in Cancers)
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21 pages, 5308 KiB  
Article
KAT2A/E2F1 Promotes Cell Proliferation and Migration via Upregulating the Expression of UBE2C in Pan-Cancer
by Shudai Lin, Li Qiu, Keying Liang, Haibo Zhang, Mingjian Xian, Zixi Chen, Jinfen Wei, Shuying Fu, Xiaocheng Gong, Ke Ding, Zihao Zhang, Bowen Hu, Xiquan Zhang, Yuyou Duan and Hongli Du
Genes 2022, 13(10), 1817; https://doi.org/10.3390/genes13101817 - 08 Oct 2022
Cited by 9 | Viewed by 2402
Abstract
Various studies have shown that lysine acetyltransferase 2A (KAT2A), E2F transcription factor 1 (E2F1), and ubiquitin conjugating enzyme E2 C (UBE2C) genes regulated the proliferation and migration of tumor cells through regulating the cell cycle. However, there [...] Read more.
Various studies have shown that lysine acetyltransferase 2A (KAT2A), E2F transcription factor 1 (E2F1), and ubiquitin conjugating enzyme E2 C (UBE2C) genes regulated the proliferation and migration of tumor cells through regulating the cell cycle. However, there is a lack of in-depth and systematic research on their mechanisms of action. This study analyzed The Cancer Genome Atlas (TCGA) to screen potential candidate genes and the regulation network of KAT2A and E2F1 complex in pan-cancer. Quantitative real-time PCR (qRT-PCR) and Western blotting (WB), cell phenotype detection, immunofluorescence co-localization, chromatin immunoprecipitation assay (ChIP), and RNA-Seq techniques were used to explore the functional of a candidate gene, UBE2C. We found that the expression of these three genes was significantly higher in more than 10 tumor types compared to normal tissue. Moreover, UBE2C was mainly expressed in tumor cells, which highlighted the impacts of UBE2C as a specific therapeutic strategy. Moreover, KAT2A and E2F1 could promote cell proliferation and the migration of cancer cells by enhancing the expression of UBE2C. Mechanically, KAT2A was found to cooperate with E2F1 and be recruited by E2F1 to the UBE2C promoter for elevating the expression of UBE2C by increasing the acetylation level of H3K9. Full article
(This article belongs to the Special Issue Gene Regulation in Cancers)
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13 pages, 4946 KiB  
Article
LHX2 Enhances the Malignant Phenotype of Esophageal Squamous Cell Carcinoma by Upregulating the Expression of SERPINE2
by Xukun Li, Xueling Wu, Hongyan Chen, Zhihua Liu, Huan He and Luhua Wang
Genes 2022, 13(8), 1457; https://doi.org/10.3390/genes13081457 - 16 Aug 2022
Cited by 5 | Viewed by 1749
Abstract
LHX2 dysregulations have been found to present in cancers, but the function of LHX2 in esophageal squamous cell carcinoma (ESCC) remains unknown. Here, we report that LHX2 was upregulated in ESCC tissues in comparison to the LHX2 levels in adjacent normal tissues. Loss- [...] Read more.
LHX2 dysregulations have been found to present in cancers, but the function of LHX2 in esophageal squamous cell carcinoma (ESCC) remains unknown. Here, we report that LHX2 was upregulated in ESCC tissues in comparison to the LHX2 levels in adjacent normal tissues. Loss- and gain-of-function experiments demonstrated that the knockdown of LHX2 markedly inhibited ESCC cells’ proliferation, migration, invasion, tumor growth and metastasis, whereas the overexpression of LHX2 had the opposite effects. A mechanistic investigation revealed that LHX2 bound to the promoter of SERPINE2 gene and transcriptionally regulated the expression of SERPINE2. Collectively, LHX2 facilitates ESCC tumor progression, and it could be a potential therapeutic target for ESCC. Full article
(This article belongs to the Special Issue Gene Regulation in Cancers)
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Review

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13 pages, 1712 KiB  
Review
CRISPR/Cas9 Genome-Editing Technology and Potential Clinical Application in Gastric Cancer
by Renata Sanches Almeida, Fernanda Wisnieski, Bruno Takao Real Karia and Marilia Arruda Cardoso Smith
Genes 2022, 13(11), 2029; https://doi.org/10.3390/genes13112029 - 04 Nov 2022
Cited by 2 | Viewed by 2232
Abstract
Gastric cancer is the subject of clinical and basic studies due to its high incidence and mortality rates worldwide. Due to the diagnosis occurring in advanced stages and the classic treatment methodologies such as gastrectomy and chemotherapy, they are extremely aggressive and limit [...] Read more.
Gastric cancer is the subject of clinical and basic studies due to its high incidence and mortality rates worldwide. Due to the diagnosis occurring in advanced stages and the classic treatment methodologies such as gastrectomy and chemotherapy, they are extremely aggressive and limit the quality of life of these patients. CRISPR/Cas9 is a tool that allows gene editing and has been used to explore the functions of genes related to gastric cancer, in addition to being used in the treatment of this neoplasm, greatly increasing our understanding of cancer genomics. In this mini-review, we seek the current status of the CRISPR/Cas9 gene-editing technology in gastric cancer research and clinical research. Full article
(This article belongs to the Special Issue Gene Regulation in Cancers)
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