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Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (17 December 2021) | Viewed by 4303

Special Issue Editors


E-Mail Website1 Website2
Guest Editor
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy
Interests: cancer; miRNAs; nanotechnology; drug delivery; nanosensors; long noncoding RNA; signal transduction; isoprenylation and cancer; aminobisphosphonates; glioblastoma; prostate cancer; hepatocellular cancer; head and neck cancer; Ras; interferons
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biochemistry, Biophysics and General Pathology, School of Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: aging; oxidative stress; nitric oxide; endothelial cells; endothelial progenitor cells; angiogenesis; inflammation; cell senescence; apoptosis; atherosclerosis; diabetes, endothelial dysfunction, sirtuins and cardiovascular disease; natural products; betaines; health; bioactive compounds; free radicals; antioxidants; ergothioneine; cell cycle; cancer-related biochemical pathways; cell proliferation; senescence; cancer cell death; epigenetic regulation; sirtuins and cancer
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania Luigi Vanvitelli, 80138 Naples, Italy
Interests: nutrition; natural products; health; bioactive compounds; free radicals; antioxidants; biochemistry of cancer; cell cycle; cancer-related biochemical pathways; cell proliferation; senescence; cancer cell death; epigenetic regulation; sirtuins and cancer; aging; oxidative stress; nitric oxide; endothelial cells; endothelial progenitor cells; angiogenesis; inflammation; cell senescence; apoptosis; atherosclerosis; endothelial dysfunction
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Precision Medicine, University of Campania “L. Vanvitelli” via L. De Crecchio 7, 80138 Naples, Italy
Interests: microRNAs; long non-coding RNAs; extracellular vesicles; regulation of gene expression; cell death mechanisms; cell signaling; cancer therapy; drug delivery systems; target therapy; immunotherapy; prostate cancer; colorectal cancer; glioblastoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announced the continuation of our Special Issue “Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases”, with a third edition.

The mechanisms of cell death have a pivotal role in the determination of the fate of normal and cancer cells in a multicellular organism. The disruption of these mechanisms is at the core of the development of inflammatory and tumor diseases, and knowledge of the molecular components altered in specific illnesses can be useful in the design of new therapeutic strategies for the treatment of human cancers as well as of inflammatory diseases. Two of the most known cell death mechanisms are apoptosis and autophagy, which are differently-involved in the regulation of tumor cell proliferation and metastasization. These mechanisms are often opposite, and autophagy is described as an escape mechanism from apoptotic occurrence, representing a protective effect of tumor cells to anti-cancer agents or hypoxic conditions, both of which are deleterious for cancer progression. On the other hand, some anti-cancer agents can induce autophagy during the repression of tumor proliferation. In this way, autophagy can become a marker of cancer response to treatment. The existence of specific tumor conditions can determine the functional role of autophagy in cancer tissues. The interaction between autophagy and apoptosis occurs through the cross-talk of the respective molecular mechanisms that are able to influence each other in a tunable way. A role for apoptosis and autophagy in the regulation of normal tissue development and differentiation is also emerging. Therefore, apoptosis and autophagy also regulate the physiological mechanisms of several organs (i.e., liver and ovary), and are involved in the occurrence of several diseases, based on either a development defect or a chronic inflammatory status. The intervention on the programmed cell death with specific agents can be a new strategy for the treatment of these kinds of diseases.

This Issue of the International Journal of Molecular Sciences will focus on the recent advances in “Apoptosis and Autophagy: The Double Edge in Cancer Development and Progression and in Other Human Diseases 3.0”, including new insights into the molecular mechanisms of apoptosis, autophagy, and other programmed cell death mechanisms (i.e., senescence), and their correlations with the control of cancer growth, metastasization, tissue development, and inflammation. Moreover, emerging data on the natural or synthetic modulators of apoptosis and autophagy in relation to new therapeutic strategies are welcome.

Prof. Dr. Michele Caraglia
Prof. Dr. Maria Luisa Balestrieri
Dr. Nunzia D’Onofrio
Dr. Amalia Luce
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • apoptosis
  • autophagy
  • cancer
  • miRNA
  • long non-coding RNAs
  • senescence
  • inflammation
  • therapeutics

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Published Papers (1 paper)

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Research

17 pages, 32333 KiB  
Article
Colorectal Cancer Apoptosis Induced by Dietary δ-Valerobetaine Involves PINK1/Parkin Dependent-Mitophagy and SIRT3
by Nunzia D’Onofrio, Elisa Martino, Luigi Mele, Antonino Colloca, Martina Maione, Domenico Cautela, Domenico Castaldo and Maria Luisa Balestrieri
Int. J. Mol. Sci. 2021, 22(15), 8117; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158117 - 29 Jul 2021
Cited by 19 | Viewed by 3623
Abstract
Understanding the mechanisms of colorectal cancer progression is crucial in the setting of strategies for its prevention. δ-Valerobetaine (δVB) is an emerging dietary metabolite showing cytotoxic activity in colon cancer cells via autophagy and apoptosis. Here, we aimed to deepen current knowledge on [...] Read more.
Understanding the mechanisms of colorectal cancer progression is crucial in the setting of strategies for its prevention. δ-Valerobetaine (δVB) is an emerging dietary metabolite showing cytotoxic activity in colon cancer cells via autophagy and apoptosis. Here, we aimed to deepen current knowledge on the mechanism of δVB-induced colon cancer cell death by investigating the apoptotic cascade in colorectal adenocarcinoma SW480 and SW620 cells and evaluating the molecular players of mitochondrial dysfunction. Results indicated that δVB reduced cell viability in a time-dependent manner, reaching IC50 after 72 h of incubation with δVB 1.5 mM, and caused a G2/M cell cycle arrest with upregulation of cyclin A and cyclin B protein levels. The increased apoptotic cell rate occurred via caspase-3 activation with a concomitant loss in mitochondrial membrane potential and SIRT3 downregulation. Functional studies indicated that δVB activated mitochondrial apoptosis through PINK1/Parkin pathways, as upregulation of PINK1, Parkin, and LC3B protein levels was observed (p < 0.0001). Together, these findings support a critical role of PINK1/Parkin-mediated mitophagy in mitochondrial dysfunction and apoptosis induced by δVB in SW480 and SW620 colon cancer cells. Full article
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