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Cell Apoptosis in Cancers: Regulation Factors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 1772

Special Issue Editor


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Guest Editor
South Texas Center of Excellence in Cancer Research, University of Texas Rio Grande Valley, Edinburg, TX, USA
Interests: cancer

Special Issue Information

Dear Colleagues,

Apoptosis is a critical process in the prevention of cancer development. The regulation factors that control apoptosis play a significant role in determining whether cancer cells survive or die. Understanding these factors and how they influence cell death can provide valuable insights for developing new strategies for cancer treatment and prevention. One key factor in the regulation of apoptosis in cancer is the balance between pro-apoptotic and anti-apoptotic proteins. Pro-apoptotic proteins promote cell death, while anti-apoptotic proteins inhibit it. Disruption of this balance can lead to uncontrolled cell growth and the development of cancer. For example, mutations in the Bcl-2 family of proteins, which regulate apoptosis, have been associated with various types of cancer. Another important factor in the regulation of cell apoptosis in cancer is the activation of specific signaling pathways such as the PI3K/Akt pathway, can regulate cell survival and apoptosis. Dysregulation of these pathways can lead to resistance to cell death and contribute to cancer progression. Targeting these signaling pathways with specific inhibitors can be an effective strategy for inducing apoptosis in cancer cells. This Special Issue will discuss the recent advances in the field, thereby contributing to our knowledge on how the selective inclusion or exclusion of key signaling pathways play a role in signal transduction, apoptosis, and cancer development or treatment.

Dr. Shabnam Malik
Guest Editor

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Keywords

  • apoptosis
  • regulation factors
  • cell death
  • cancer
  • treatment

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Published Papers (1 paper)

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Research

21 pages, 4467 KiB  
Article
DEAD/H Box 5 (DDX5) Augments E2F1-Induced Cell Death Independent of the Tumor Suppressor p53
by Rinka Nakajima, Yaxuan Zhou, Mashiro Shirasawa, Naoyasu Nishimura, Lin Zhao, Mariana Fikriyanti, Yuki Kamiya, Ritsuko Iwanaga, Andrew P. Bradford, Kaori Shinmyozu, Gohei Nishibuchi, Jun-ichi Nakayama, Kenta Kurayoshi, Keigo Araki and Kiyoshi Ohtani
Int. J. Mol. Sci. 2024, 25(24), 13251; https://doi.org/10.3390/ijms252413251 - 10 Dec 2024
Cited by 1 | Viewed by 1118
Abstract
In almost all cancers, the p53 pathway is disabled and cancer cells survive. Hence, it is crucially important to induce cell death independent of p53 in the treatment of cancers. The transcription factor E2F1 is controlled by binding of the tumor suppressor pRB, [...] Read more.
In almost all cancers, the p53 pathway is disabled and cancer cells survive. Hence, it is crucially important to induce cell death independent of p53 in the treatment of cancers. The transcription factor E2F1 is controlled by binding of the tumor suppressor pRB, and induces apoptosis by activating the ARF gene, an upstream activator of p53, when deregulated from pRB by loss of pRB function. Deregulated E2F1 can also induce apoptosis, independent of p53, via other targets such as TAp73 and BIM. We searched for novel E2F1-interacting proteins and identified the RNA helicase DEAD/H box 5 (DDX5), which also functions as a transcriptional coactivator. In contrast to the reported growth-promoting roles of DDX5, we show that DDX5 suppresses cell growth and survival by augmentation of deregulated E2F1 activity. Over-expression of DDX5 enhanced E2F1 induction of tumor suppressor gene expression and cell death. Conversely, shRNA-mediated knockdown of DDX5 compromised both. Moreover, DDX5 modulated E2F1-mediated cell death independent of p53, for which DDX5 also functions as a coactivator. Since p53 function is disabled in almost all cancers, these results underscore the roles of DDX5 in E2F1-mediated induction of cell death, independent of p53, and represent novel aspects for the treatment of p53-disabled cancer cells. Full article
(This article belongs to the Special Issue Cell Apoptosis in Cancers: Regulation Factors)
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