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New Molecules Modulating Autophagy in Cancers
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New Molecules Modulating Autophagy in Cancers

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

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 12341

Special Issue Editor

Prof. Dr. Daniela Trisciuoglio

E-Mail Website
Guest Editor
Department of Research, Advanced Diagnostics and Technological Innovation, Regina Elena National Cancer Institute, Rome, Italy
Interests: cancer; epigenetic drugs; protein acetylation; cell death and autophagy; combination therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionarily conserved cellular catabolic process that facilitates nutrient recycling from damaged organelles and other cellular components through lysosomal degradation. Deregulation of this process is associated with several pathological processes, including cancer. For this reason, targeting of autophagy is a promising novel therapeutic approach with broad applications in cancer therapy. Nevertheless, autophagy has a dual role in cancer acting as cytoprotective or cytotoxic; thus, the identification of the role of autophagy in each tumor context is crucial.

We welcome articles focused on new or old molecules that modulating autophagic pathway can induce cell death or augments the efficacy of anticancer agents in various cancers. Reviews on recent advances in the development of autophagy modulators for cancer treatment will be also included in this special issue.

Prof. Dr. Daniela Trisciuoglio
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • autophagy
  • chemoresistance
  • cancer therapy
  • autophagy inhibitors
  • drug resistance
  • autophagy activators
  • autophagic cell death
  • autophagy biomarkers

Published Papers (3 papers)

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Research

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20 pages, 5798 KiB  
Article
In Pancreatic Adenocarcinoma Alpha-Synuclein Increases and Marks Peri-Neural Infiltration
by Matteo Bianchini, Maria Giambelluca, Maria Concetta Scavuzzo, Gregorio Di Franco, Simone Guadagni, Matteo Palmeri, Niccolò Furbetta, Desirée Gianardi, Aurelio Costa, Manuel Gentiluomo, Raffaele Gaeta, Luca Emanuele Pollina, Alfredo Falcone, Caterina Vivaldi, Giulio Di Candio, Francesca Biagioni, Carla Letizia Busceti, Paola Soldani, Stefano Puglisi-Allegra, Luca Morelli and Francesco Fornaiadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2022, 23(7), 3775; https://doi.org/10.3390/ijms23073775 - 29 Mar 2022
Cited by 5 | Viewed by 1963
Abstract
α-Synuclein (α-syn) is a protein involved in neuronal degeneration. However, the family of synucleins has recently been demonstrated to be involved in the mechanisms of oncogenesis by selectively accelerating cellular processes leading to cancer. Pancreatic ductal adenocarcinoma (PDAC) is one of the most [...] Read more.
α-Synuclein (α-syn) is a protein involved in neuronal degeneration. However, the family of synucleins has recently been demonstrated to be involved in the mechanisms of oncogenesis by selectively accelerating cellular processes leading to cancer. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human cancers, with a specifically high neurotropism. The molecular bases of this biological behavior are currently poorly understood. Here, α-synuclein was analyzed concerning the protein expression in PDAC and the potential association with PDAC neurotropism. Tumor (PDAC) and extra-tumor (extra-PDAC) samples from 20 patients affected by PDAC following pancreatic resections were collected at the General Surgery Unit, University of Pisa. All patients were affected by moderately or poorly differentiated PDAC. The amount of α-syn was compared between tumor and extra-tumor specimen (sampled from non-affected neighboring pancreatic areas) by using in situ immuno-staining with peroxidase anti-α-syn immunohistochemistry, α-syn detection by using Western blotting, and electron microscopy by using α-syn-conjugated immuno-gold particles. All the methods consistently indicate that each PDAC sample possesses a higher amount of α-syn compared with extra-PDAC tissue. Moreover, the expression of α-syn was much higher in those PDAC samples from tumors with perineural infiltration compared with tumors without perineural infiltration. Full article
(This article belongs to the Special Issue New Molecules Modulating Autophagy in Cancers)
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Review

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19 pages, 1835 KiB  
Review
The Potential of Epigallocatechin Gallate (EGCG) in Targeting Autophagy for Cancer Treatment: A Narrative Review
by Elena Ferrari, Saverio Bettuzzi and Valeria Naponelli
Int. J. Mol. Sci. 2022, 23(11), 6075; https://doi.org/10.3390/ijms23116075 - 28 May 2022
Cited by 31 | Viewed by 3805
Abstract
Autophagy is an evolutionarily conserved process for the degradation of redundant or damaged cellular material by means of a lysosome-dependent mechanism, contributing to cell homeostasis and survival. Autophagy plays a multifaceted and context-dependent role in cancer initiation, maintenance, and progression; it has a [...] Read more.
Autophagy is an evolutionarily conserved process for the degradation of redundant or damaged cellular material by means of a lysosome-dependent mechanism, contributing to cell homeostasis and survival. Autophagy plays a multifaceted and context-dependent role in cancer initiation, maintenance, and progression; it has a tumor suppressive role in the absence of disease and is upregulated in cancer cells to meet their elevated metabolic demands. Autophagy represents a promising but challenging target in cancer treatment. Green tea is a widely used beverage with healthy effects on several diseases, including cancer. The bioactive compounds of green tea are mainly catechins, and epigallocatechin-gallate (EGCG) is the most abundant and biologically active among them. In this review, evidence of autophagy modulation and anti-cancer effects induced by EGCG treatment in experimental cancer models is presented. Reviewed articles reveal that EGCG promotes cytotoxic autophagy often through the inactivation of PI3K/Akt/mTOR pathway, resulting in apoptosis induction. EGCG pro-oxidant activity has been postulated to be responsible for its anti-cancer effects. In combination therapy with a chemotherapy drug, EGCG inhibits cell growth and the drug-induced pro-survival autophagy. The selected studies rightly claim EGCG as a valuable agent in cancer chemoprevention. Full article
(This article belongs to the Special Issue New Molecules Modulating Autophagy in Cancers)
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35 pages, 6393 KiB  
Review
Autophagy Modulators in Cancer Therapy
by Kamila Buzun, Agnieszka Gornowicz, Roman Lesyk, Krzysztof Bielawski and Anna Bielawska
Int. J. Mol. Sci. 2021, 22(11), 5804; https://doi.org/10.3390/ijms22115804 - 28 May 2021
Cited by 44 | Viewed by 5669
Abstract
Autophagy is a process of self-degradation that plays an important role in removing damaged proteins, organelles or cellular fragments from the cell. Under stressful conditions such as hypoxia, nutrient deficiency or chemotherapy, this process can also become the strategy for cell survival. Autophagy [...] Read more.
Autophagy is a process of self-degradation that plays an important role in removing damaged proteins, organelles or cellular fragments from the cell. Under stressful conditions such as hypoxia, nutrient deficiency or chemotherapy, this process can also become the strategy for cell survival. Autophagy can be nonselective or selective in removing specific organelles, ribosomes, and protein aggregates, although the complete mechanisms that regulate aspects of selective autophagy are not fully understood. This review summarizes the most recent research into understanding the different types and mechanisms of autophagy. The relationship between apoptosis and autophagy on the level of molecular regulation of the expression of selected proteins such as p53, Bcl-2/Beclin 1, p62, Atg proteins, and caspases was discussed. Intensive studies have revealed a whole range of novel compounds with an anticancer activity that inhibit or activate regulatory pathways involved in autophagy. We focused on the presentation of compounds strongly affecting the autophagy process, with particular emphasis on those that are undergoing clinical and preclinical cancer research. Moreover, the target points, adverse effects and therapeutic schemes of autophagy inhibitors and activators are presented. Full article
(This article belongs to the Special Issue New Molecules Modulating Autophagy in Cancers)
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