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Biomolecules
Special Issues
Molecular Signalling Pathways in Tumorigenesis and Tumor Suppression
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Molecular Signalling Pathways in Tumorigenesis and Tumor Suppression

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1680

Special Issue Editor

Dr. Kiyoshi Ohtani

E-Mail Website
Guest Editor
Department of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda 669-1330, Hyogo, Japan
Interests: cancer cell biology; RB; E2F; ARF; p53
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am pleased to invite you to contribute to this Special Issue, entitled “Molecular Signalling Pathways in Tumorigenesis and Tumor Suppression”. The main obstacles in the radical treatment of cancers are side effects caused by damage to normal growing cells. To avoid these side effects, we must specifically target cancer cells to preserve normal-growing cells. For this purpose, the unique properties of cancer cells caused by oncogenic changes, which facilitate aberrant cell growth and disable the tumor suppressive mechanism, could be fascinating targets. For example, in almost all cancers, the two major tumor suppressive pathways, the RB pathway and the p53 pathway, are disabled, and the activity of the transcription factor E2F, the principal target of RB, is enhanced. To utilize the unique properties of cancer cells, we must deepen our understanding of the molecular signalling pathways involved in tumorigenesis and tumor suppression. The changes in these pathways may represent unique features of cancer cells, which can be utilized to specifically target cancer cells to avoid side effects.

This Special Issue will explore the molecular signalling pathways involved in tumorigenesis and tumor suppression in cancer cells and normal cells, seeking unique properties of cancer cells to specifically target cancer cells. Original research articles and reviews are welcome.

I look forward to receiving your contributions.

Dr. Kiyoshi Ohtani
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 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. Biomolecules 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 2700 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

  • E2F
  • RB
  • p53
  • cancer
  • tumor suppression

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Published Papers (1 paper)

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Research

21 pages, 2077 KiB  
Article
The N-Terminal Region of the Transcription Factor E2F1 Contains a Novel Transactivation Domain and Recruits General Transcription Factor GTF2H2
by Lin Zhao, Rinka Nakajima, Yaxuan Zhou, Mashiro Shirasawa, Mariana Fikriyanti, Yuki Kamiya, Hiroyuki Toh, Hideyuki Komori, Ritsuko Iwanaga, Andrew P. Bradford, Hideo Nishitani, Kenta Kurayoshi, Keigo Araki and Kiyoshi Ohtani
Biomolecules 2024, 14(11), 1357; https://doi.org/10.3390/biom14111357 - 25 Oct 2024
Cited by 1 | Viewed by 1224
Abstract
The transcription factor E2F1 is the principal target of the tumor suppressor pRB. E2F1 promotes cell proliferation by activating growth-promoting genes upon growth stimulation. In contrast, E2F1 contributes to tumor suppression by activating tumor suppressor genes, such as ARF, upon loss of [...] Read more.
The transcription factor E2F1 is the principal target of the tumor suppressor pRB. E2F1 promotes cell proliferation by activating growth-promoting genes upon growth stimulation. In contrast, E2F1 contributes to tumor suppression by activating tumor suppressor genes, such as ARF, upon loss of pRB function, a major oncogenic change. The transactivation domain of E2F1 has previously been mapped to the C-terminal region. We show here that the N-terminal region of E2F1 is critical for the activation of tumor suppressor genes. Deletion of the N-terminal region dramatically compromised E2F1 activation of tumor suppressor genes. The N-terminal region showed transactivation ability when fused to the DNA-binding domain of GAL4. A search for novel interacting factors with the N-terminal region, using a yeast two-hybrid system, identified the general transcription factor GTF2H2. Overexpression of GTF2H2 enhanced E2F1 activation of tumor suppressor genes and induction of cell death. Conversely, the knockdown of GTF2H2 compromised both. E2F1 binding enhanced the binding of GTF2H2 to target promoters depending on the integrity of the N-terminal region. Taken together, these results suggest that the N-terminal region of E2F1 contains a novel transactivation domain that mediates the activation of tumor suppressor genes, at least in part, by recruiting GTF2H2. Full article
(This article belongs to the Special Issue Molecular Signalling Pathways in Tumorigenesis and Tumor Suppression)
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