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Current Molecular Advances in Apoptosis

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

Deadline for manuscript submissions: 31 January 2027 | Viewed by 733

Special Issue Editors


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Department of Translational Medical Sciences, University of Campania, 80131 Naples, Italy
Interests: nephrology; chaotic systems
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Special Issue Information

Dear Colleagues,

Apoptosis is a vital mechanism for maintaining tissue integrity, immune balance, and proper development. Core apoptotic components include caspases, mitochondrial cytochrome c release, and chromatin condensation. However, recent studies highlight caspase-independent pathways involving apoptosis-inducing factor (AIF) and endonuclease G. Circulating biomarkers like cell-free DNA and cytokeratin-18 now allow the better monitoring of apoptotic activity in vivo. Apoptosis dysregulation is linked not only to cancer, neurodegeneration, and glomerulonephritis, but also to aging. This Special Issue explores apoptosis within a broader context of regulated cell death, including necroptosis, ferroptosis, pyroptosis, and NETosis, revealing their interconnected roles in inflammation and disease. A particularly intriguing feature of apoptosis is how DNA cleavage by CAD (Caspase-Activated DNase) induces unique chromatin condensation, suggesting that DNA length may physically restrict compaction. By addressing emerging molecular pathways, death modalities, and diagnostic tools, this Special Issue aims to foster innovative approaches to target apoptosis and related mechanisms for therapeutic benefit.

Dr. Mariarosaria Boccellino
Dr. Davide Viggiano
Guest Editors

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Keywords

  • apoptosis
  • glomerulonephritis
  • aging
  • caspase
  • endonuclease
  • DNA
  • cytokeratin

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Published Papers (1 paper)

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Research

11 pages, 4458 KB  
Article
Phenformin-Induced Apoptosis: A Potential Mechanism for Cervical Cancer Cell Inhibition
by Gehad M. Subaiea, Yernar Amangelsin, Kamila Sagatbekova, Ahmed A. Katamesh, Sameer A. Alkubati, Ahmed A. Alobaida, Hanan Abdelmawgoud Atia, Nasrin E. Khalifa, Thamir M. Alshammari, Reezal Ishak and Mohamad Aljofan
Int. J. Mol. Sci. 2026, 27(11), 4941; https://doi.org/10.3390/ijms27114941 - 29 May 2026
Viewed by 162
Abstract
Phenformin, a representative of the biguanides class was previously used for treatment of type 2 diabetes and discontinued due to a risk of causing lactic acidosis, has shown promising anticancer activity in numerous studies. Since many types of cancer arise and proliferate due [...] Read more.
Phenformin, a representative of the biguanides class was previously used for treatment of type 2 diabetes and discontinued due to a risk of causing lactic acidosis, has shown promising anticancer activity in numerous studies. Since many types of cancer arise and proliferate due to dysregulation in apoptotic or autophagic pathways, this study aimed to assess the underlying anticancer effects of phenformin in terms of these two processes. We initially set out to examine the antiproliferative effects of phenformin on multiple cancer cell lines including breast, pancreatic, cervical cancers, hepatocellular carcinoma and malignant melanoma. Subsequently, the expression of apoptosis and autophagy related proteins was measured in the cervical cancer cell lines found to be the most susceptible to antiproliferative effects of phenformin. Additionally, the ability of phenformin to potentiate the antitumor effect of resveratrol and vistusertib was assessed. Phenformin increased the expression of pro-apoptotic factor, Bax, and lowered the level of anti-apoptotic protein, Bcl-2. Hence, it was proposed that phenformin promotes antiproliferative activity by inducing apoptosis. Our findings demonstrate that phenformin decreases the proliferation of various cancer cell lines in a dose-dependent manner and may have an ability to increase the autophagic flux in cervical cancer cells. Our findings demonstrate that phenformin decreases the proliferation of various cancer cell lines in a dose-dependent manner potentially by inducing apoptosis. Full article
(This article belongs to the Special Issue Current Molecular Advances in Apoptosis)
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