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Cancers
Special Issues
Transcription Factor Regulation and Activities in Cancer
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Transcription Factor Regulation and Activities in Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 11281

Special Issue Editor

Prof. Dr. Scott A. Ness

E-Mail Website
Guest Editor
Department of Internal Medicine, Comprehensive Cancer Center, University of New Mexico, Albuquerque, NM 87109, USA
Interests: MYB oncogene; transcriptional regulation; leukemia; adenoid cystic carcinoma; genomics

Special Issue Information

Dear Colleagues, 

Although many oncogenes encode transcription factors, genomic approaches have shown that oncogene transcription factors regulate hundreds or thousands of genes in tumors. Consequently, how a transcription factor actually becomes an oncogene is not clear. Do oncogene transcription factors regulate one or a few key targets that induce transformation, or do they induce a transformed phenotype by causing hundreds or thousands of changes that reprogram cells? How do oncogenic transcription factors reorganize chromatin to affect hundreds or thousands of genes across the genome? This Special Issue will focus on the regulatory mechanisms that change the expression or activities of oncogenic transcription factors and on the downstream epigenetic and transcriptional changes that are induced and that lead to cell preprogramming during transformation and oncogenesis.

Prof. Dr. Scott A. Ness
Guest Editor

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
  • epigenetics
  • cellular reprogramming
  • nuclear imaging
  • signaling to the nucleus

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Published Papers (3 papers)

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Research

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21 pages, 32785 KiB  
Article
Dynamic Visualization of TGF-β/SMAD3 Transcriptional Responses in Single Living Cells
by Dieuwke L. Marvin, Li You, Laura Bornes, Maarten van Dinther, Niek Peters, Hao Dang, Sarah K. Hakuno, Marten Hornsveld, Onno Kranenburg, Jacco van Rheenen, Jos H. T. Rohling, Miao-Ping Chien, Peter ten Dijke and Laila Ritsma
Cancers 2022, 14(10), 2508; https://doi.org/10.3390/cancers14102508 - 19 May 2022
Cited by 6 | Viewed by 3730
Abstract
Transforming growth factor-β (TGF-β) signaling is tightly controlled in duration and intensity during embryonic development and in the adult to maintain tissue homeostasis. To visualize the TGF-β/SMAD3 signaling kinetics, we developed a dynamic TGF-β/SMAD3 transcriptional fluorescent reporter using multimerized SMAD3/4 binding elements driving [...] Read more.
Transforming growth factor-β (TGF-β) signaling is tightly controlled in duration and intensity during embryonic development and in the adult to maintain tissue homeostasis. To visualize the TGF-β/SMAD3 signaling kinetics, we developed a dynamic TGF-β/SMAD3 transcriptional fluorescent reporter using multimerized SMAD3/4 binding elements driving the expression of a quickly folded and highly unstable GFP protein. We demonstrate the specificity and sensitivity of this reporter and its wide application to monitor dynamic TGF-β/SMAD3 transcriptional responses in both 2D and 3D systems in vitro, as well as in vivo, using live-cell and intravital imaging. Using this reporter in B16F10 cells, we observed single cell heterogeneity in response to TGF-β challenge, which can be categorized into early, late, and non-responders. Because of its broad application potential, this reporter allows for new discoveries into how TGF-β/SMAD3-dependent transcriptional dynamics are affected during multistep and reversible biological processes. Full article
(This article belongs to the Special Issue Transcription Factor Regulation and Activities in Cancer)
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19 pages, 4831 KiB  
Article
Bcr-TMP, a Novel Nanomolar-Active Compound That Exhibits Both MYB- and Microtubule-Inhibitory Activity
by Maria V. Yusenko, Abhiruchi Biyanee, Daria Frank, Leonhard H. F. Köhler, Mattias K. Andersson, Cyrus Khandanpour, Rainer Schobert, Göran Stenman, Bernhard Biersack and Karl-Heinz Klempnauer
Cancers 2022, 14(1), 43; https://doi.org/10.3390/cancers14010043 - 23 Dec 2021
Cited by 12 | Viewed by 3105
Abstract
Studies of the role of MYB in human malignancies have highlighted MYB as a potential drug target for acute myeloid leukemia (AML) and adenoid cystic carcinoma (ACC). Here, we present the initial characterization of 2-amino-4-(3,4,5-trimethoxyphenyl)-4H-naphtho[1,2-b]pyran-3-carbonitrile (Bcr-TMP), a nanomolar-active MYB-inhibitory [...] Read more.
Studies of the role of MYB in human malignancies have highlighted MYB as a potential drug target for acute myeloid leukemia (AML) and adenoid cystic carcinoma (ACC). Here, we present the initial characterization of 2-amino-4-(3,4,5-trimethoxyphenyl)-4H-naphtho[1,2-b]pyran-3-carbonitrile (Bcr-TMP), a nanomolar-active MYB-inhibitory compound identified in a screen for novel MYB inhibitors. Bcr-TMP affects MYB function in a dual manner by inducing its degradation and suppressing its transactivation potential by disrupting its cooperation with co-activator p300. Bcr-TMP also interferes with the p300-dependent stimulation of C/EBPβ, a transcription factor co-operating with MYB in myeloid cells, indicating that Bcr-TMP is a p300-inhibitor. Bcr-TMP reduces the viability of AML cell lines at nanomolar concentrations and induces cell-death and expression of myeloid differentiation markers. It also down-regulates the expression of MYB target genes and exerts stronger anti-proliferative effects on MYB-addicted primary murine AML cells and patient-derived ACC cells than on their non-oncogenic counterparts. Surprisingly, we observed that Bcr-TMP also has microtubule-disrupting activity, pointing to a possible link between MYB-activity and microtubule stability. Overall, Bcr-TMP is a highly potent multifunctional MYB-inhibitory agent that warrants further investigation of its therapeutic potential and mechanism(s) of action. Full article
(This article belongs to the Special Issue Transcription Factor Regulation and Activities in Cancer)
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Review

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21 pages, 1754 KiB  
Review
Disruption of Tumor Suppressors HNF4α/HNF1α Causes Tumorigenesis in Liver
by Aamir Salam Teeli, Kamila Łuczyńska, Effi Haque, Mohmmad Abrar Gayas, Dawid Winiarczyk and Hiroaki Taniguchi
Cancers 2021, 13(21), 5357; https://doi.org/10.3390/cancers13215357 - 26 Oct 2021
Cited by 6 | Viewed by 3865
Abstract
The hepatocyte nuclear factor-4α (HNF4α) and hepatocyte nuclear factor-1α (HNF1α) are transcription factors that influence the development and maintenance of homeostasis in a variety of tissues, including the liver. As such, disruptions in their transcriptional networks can herald a number of pathologies, such [...] Read more.
The hepatocyte nuclear factor-4α (HNF4α) and hepatocyte nuclear factor-1α (HNF1α) are transcription factors that influence the development and maintenance of homeostasis in a variety of tissues, including the liver. As such, disruptions in their transcriptional networks can herald a number of pathologies, such as tumorigenesis. Largely considered tumor suppressants in liver cancer, these transcription factors regulate key events of inflammation, epithelial–mesenchymal transition, metabolic reprogramming, and the differentiation status of the cell. High-throughput analysis of cancer cell genomes has identified a number of hotspot mutations in HNF1α and HNF4α in liver cancer. Such results also showcase HNF1α and HNF4α as important therapeutic targets helping us step into the era of personalized medicine. In this review, we update current findings on the roles of HNF1α and HNF4α in liver cancer development and progression. It covers the molecular mechanisms of HNF1α and HNF4α dysregulation and also highlights the potential of HNF4α as a therapeutic target in liver cancer. Full article
(This article belongs to the Special Issue Transcription Factor Regulation and Activities in Cancer)
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