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Molecular Mechanisms of Cancer Cell Death
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Molecular Mechanisms of Cancer Cell Death

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 5763

Special Issue Editors

Dr. Bor-Chyuan Su

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
Interests: cell death; signal transduction; cancer biology
Dr. Hsin-Hsien Yu

E-Mail Website
Guest Editor
Department of Surgery, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan
Interests: surgical oncology; gastric cancer research; peritoneal surface malignancy; cytoreductive surgery and hyperthermic intraperitoneal chemotherapy; laparoscopic and robotic digestive surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The main approach to cancer treatment is to specifically cause death in tumor cells. This aim can be met by inducing any of the three major forms of cell death, including apoptosis, autophagy, and necrosis, via distinct molecular mechanisms. Although the induction of any form of cell death can be effective as an anticancer strategy, the roles of each pathway in cancer therapy are complex and often context dependent. In addition, it is not uncommon for cancer cells to develop resistance to therapy-induced cell death. Thus, a deep understanding of how cancer therapeutics affect the regulatory pathways of cell death will allow researchers to develop more precise and effective anticancer strategies.

For this Special Issue, appropriate research topics include cancer cell death regulation, novel therapeutic targets, molecular mechanisms, and drug (therapy) resistance.

Dr. Bor-Chyuan Su
Dr. Hsin-Hsien Yu
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. Current Issues in Molecular Biology 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 2200 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

  • cell death
  • anti-cancer agents
  • signal transduction
  • chemoresistance
  • therapeutic resistance
  • apoptosis
  • autophagy
  • necrosis

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Published Papers (2 papers)

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Research

19 pages, 4810 KiB  
Article
The Identification of New c-FLIP Inhibitors for Restoring Apoptosis in TRAIL-Resistant Cancer Cells
by Katherine Yaacoub, Rémy Pedeux, Pierre Lafite, Ulrich Jarry, Samia Aci-Sèche, Pascal Bonnet, Richard Daniellou and Thierry Guillaudeux
Curr. Issues Mol. Biol. 2024, 46(1), 710-728; https://doi.org/10.3390/cimb46010046 - 12 Jan 2024
Cited by 4 | Viewed by 3353
Abstract
The catalytically inactive caspase-8-homologous protein, c-FLIP, is a potent antiapoptotic protein highly expressed in various types of cancers. c-FLIP competes with caspase-8 for binding to the adaptor protein FADD (Fas-Associated Death Domain) following death receptors’ (DRs) activation via the ligands of the TNF-R [...] Read more.
The catalytically inactive caspase-8-homologous protein, c-FLIP, is a potent antiapoptotic protein highly expressed in various types of cancers. c-FLIP competes with caspase-8 for binding to the adaptor protein FADD (Fas-Associated Death Domain) following death receptors’ (DRs) activation via the ligands of the TNF-R family. As a consequence, the extrinsic apoptotic signaling pathway involving DRs is inhibited. The inhibition of c-FLIP activity in tumor cells might enhance DR-mediated apoptosis and overcome immune and anticancer drug resistance. Based on an in silico approach, the aim of this work was to identify new small inhibitory molecules able to bind selectively to c-FLIP and block its anti-apoptotic activity. Using a homology 3D model of c-FLIP, an in silico screening of 1880 compounds from the NCI database (National Cancer Institute) was performed. Nine molecules were selected for in vitro assays, based on their binding affinity to c-FLIP and their high selectivity compared to caspase-8. These molecules selectively bind to the Death Effector Domain 2 (DED2) of c-FLIP. We have tested in vitro the inhibitory effect of these nine molecules using the human lung cancer cell line H1703, overexpressing c-FLIP. Our results showed that six of these newly identified compounds efficiently prevent FADD/c-FLIP interactions in a molecular pull-down assay, as well as in a DISC immunoprecipitation assay. The overexpression of c-FLIP in H1703 prevents TRAIL-mediated apoptosis; however, a combination of TRAIL with these selected molecules significantly restored TRAIL-induced cell death by rescuing caspase cleavage and activation. Altogether, our findings indicate that new inhibitory chemical molecules efficiently prevent c-FLIP recruitment into the DISC complex, thus restoring the caspase-8-dependent apoptotic cascade. These results pave the way to design new c-FLIP inhibitory molecules that may serve as anticancer agents in tumors overexpressing c-FLIP. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Cell Death)
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14 pages, 3798 KiB  
Article
Cucurbitacin E Exerts Anti-Proliferative Activity via Promoting p62-Dependent Apoptosis in Human Non-Small-Cell Lung Cancer A549 Cells
by Han-Lin Hsu, Bo-Jyun Lin, Yu-Chen Lin, Chih-Chieh Tu, Nham-Linh Nguyen, Ching-Chiung Wang, Mei-Chuan Chen and Chun-Han Chen
Curr. Issues Mol. Biol. 2023, 45(10), 8138-8151; https://doi.org/10.3390/cimb45100514 - 7 Oct 2023
Cited by 3 | Viewed by 1817
Abstract
EGFR tyrosine kinase inhibitors (TKIs) are the first-line treatment for advanced EGFR-mutated non-small-cell lung cancer (NSCLC). However, NSCLC patients with wild-type EGFR and KRAS mutation are ineligible for EGFR-TKIs. Therefore, the discovery of new therapeutic agents is urgently needed for NSCLC patients who [...] Read more.
EGFR tyrosine kinase inhibitors (TKIs) are the first-line treatment for advanced EGFR-mutated non-small-cell lung cancer (NSCLC). However, NSCLC patients with wild-type EGFR and KRAS mutation are ineligible for EGFR-TKIs. Therefore, the discovery of new therapeutic agents is urgently needed for NSCLC patients who cannot receive targeted therapies. Natural products possess tremendous chemical diversity and have been extensively investigated for their anticancer activity. In this study, we found that Cucurbitacin E (Cu E), a triterpene of cucurbitacins widely presented in the edible plants of the Cucurbitaceae family, significantly inhibits the viability and proliferation of A549 cells that harbor wild-type EGFR and KRAS mutation. Our results revealed that Cu E increases cell-cycle arrest at G2/M and subG1 phase. Mechanistically, Cu E significantly inhibits the phosphorylation and protein levels of regulatory proteins and hinders G2/M cell-cycle progression. Meanwhile, the treatment of Cu E resulted in DNA damage response and apoptosis. For the first time, we observed that Cu E induces incomplete autophagy as evidenced by increased LC3B-II expression and p62-accumulation. Knockdown of p62 rescued the cells from Cu E-mediated anti-proliferative effect, apoptosis, DNA damage, and ROS production. These findings suggest that Cu E is a promising drug candidate for NSCLC. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Cell Death)
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