Transcription Factor E2F in Normal and Cancer Cells

Dear Colleagues,

I am pleased to invite you to contribute to this Special Issue “Transcription Factor E2F in Normal and Cancer Cells”. As the principal target of the tumor suppressor pRB, E2F plays crucial roles in many important biological processes such as cell proliferation, DNA repair, tumorigenesis, apoptosis, cellular senescence, tumor suppression, development, differentiation, metabolism, stemness, invasion, metastasis, angiogenesis and others. The main obstacles in the radical treatment of cancers are side effects caused by the damage to normal growing cells. To avoid these side effects, we have to specifically target cancer cells. In almost all cancers, the RB pathway is disabled due to oncogenic changes, and the E2F activity is enhanced. Hence, many of the biological processes mentioned above may be affected and may represent a unique feature of cancer cells, which can be utilized to specifically target cancer cells to avoid side effects.

This Special Issue aims to explore E2F-based changes in cancer cells and also in normal cells upon oncogenic changes, seeking new approaches to specifically target cancer cells. Original research articles and reviews are welcome.

I look forward to receiving your contributions.

Prof. 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.

• E2F
• RB
• p53
• cancer
• tumor suppression

Title: The N-terminal region of the transcription factor E2F1 contains novel transactivation domain and recruits general transcription factor GTF2H2
Authors: Kiyoshi Ohtani
Affiliation: Department of Biomedical Sciences, School of Biological and Environmental Sciences, Kwansei Gakuin University, 1 Gakuen Uegahara, Sanda, Hyogo 669-1330, Japan
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 pRB function, a major oncogenic change. Transactivation domain of E2F1 has been mapped at the C-terminal region. We show here that the N-terminal region of E2F1 plays crucial roles in activation of tumor suppressor genes. Deletion of the N-terminal region of E2F1 dramatically compromised ability to activate tumor suppressor genes. The N-terminal region showed transactivation ability when fused to DNA biding domain of GAL4. We searched for novel interacting factors with the N-terminal region using yeast two-hybrid system and identified the general transcription factor GTF2H2. Over-expression of GTF2H2 enhanced E2F1-mediated induction of tumor suppressor gene expression and cell death. Conversely, knockdown of GTF2H2 compromised the induction of tumor suppressor gene expression and cell death. E2F1 binding enhanced binding of GTF2H2 to target promoters. Taken together, these results suggest that the N-terminal region of E2F1 contains novel transactivation domain and contributes to activation of tumor suppressor genes by, at least in part, interacting with GTF2H2.