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Cancers
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Autophagy–EMT Interrelations: At the Core of Tumor Transformation
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Autophagy–EMT Interrelations: At the Core of Tumor Transformation

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 9850

Special Issue Editors

Dr. Marco Cordani

E-Mail Website
Guest Editor
1. Department of Biochemistry and Molecular Biology, School of Biology, Complutense University, 28040 Madrid, Spain
2. Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain
Interests: nanomedicine; cancer therapy; ROS; autophagy; chemotherapy
Special Issues, Collections and Topics in MDPI journals
Dr. Miguel Sánchez Álvarez

E-Mail Website
Guest Editor
Cell and Developmental Biology Area, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain
Interests: lipid droplets; ER stress; UPR; autophagy; mechanotrasduction
Dr. Raffaele Strippoli

E-Mail Website
Guest Editor
Department of Molecular Medicine, Sapienza University of Rome, Rome, Italy
Interests: peritoneal fibrosis; EMT; biomechanical remodeling; epigenetics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Stefania Meschini

E-Mail Website
Guest Editor
National Center for Drug Research and Evaluation, National Institute of Health, Viale Regina Elena, 00161 Rome, Italy
Interests: ultrastructural pathology; nanomedicine; nanotoxicology; cell biology; anticancer therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Condello

E-Mail Website
Guest Editor
National Center for Drug Research and Evaluation, National Institute of Health, Viale Regina Elena, 00161 Rome, Italy
Interests: characterization of multidrug-resistant tumor cells; in vitro study of apoptosis induced by chemotherapeutic drugs; in vitro study of autophagy (cell survival mechanism or type II programmed cell death); in vitro study of new anticancer strategies based on the use of natural products in combination with drugs, on electrochemotherapy, and on liposomes; study of interaction between cells and metal nanoparticles (ZnO or Ag-NPs) to investigate nanotoxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Autophagy and EMT are two major processes in cancer which share common signaling pathways and are linked by complex interrelations. The journal Cancers encourages the submission of both reviews and original articles focusing on the molecular mechanisms regulating autophagy–EMT interplay and how these oncogenic nodes can affect cancer development and progression. This Special Issue is aimed at providing high-quality contributions on the latest advances describing cytoskeleton–mitochondria dynamics, control of EMT by autophagy and vice versa, oxidative and nutritional response, hypoxia, epigenetic mechanisms, new drugs, and new methods of pharmacological delivery, including nanomedicine. Potential topics include but are not limited to:  

  • Identifying the molecular mediators that link autophagy and EMT in cancer;
  • Understanding the role of structural proteins (including cadherins and integrins) in controlling autophagy in response to EMT activation in tumor cells;
  • Dissecting how mitochondrial dynamics affects cellular architecture during EMT and metastatic spreading;
  • Shedding light on how the molecular interplay between autophagy and EMT influences cancer development and progression.  

The collection of manuscripts will be published as a Special Issue of the journal.

Dr. Marco Cordani
Dr. Miguel Sánchez Álvarez
Dr. Raffaele Strippoli
Prof. Dr. Stefania Meschini
Dr. Maria Condello
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • autophagy
  • EMT
  • TGF-beta
  • cytoskeleton
  • mitochondria
  • signaling pathways
  • cancer progression

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

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15 pages, 3182 KiB  
Article
High G9a Expression in DLBCL and Its Inhibition by Niclosamide to Induce Autophagy as a Therapeutic Approach
by Chin-Mu Hsu, Kung-Chao Chang, Tzer-Ming Chuang, Man-Ling Chu, Pei-Wen Lin, Hsiao-Sheng Liu, Shih-Yu Kao, Yi-Chang Liu, Chien-Tzu Huang, Min-Hong Wang, Tsung-Jang Yeh, Yuh-Ching Gau, Jeng-Shiun Du, Hui-Ching Wang, Shih-Feng Cho, Chi-En Hsiao, Yuhsin Tsai, Samuel Yien Hsiao, Li-Chuan Hung, Chia-Hung Yen and Hui-Hua Hsiaoadd Show full author list remove Hide full author list
Cancers 2023, 15(16), 4150; https://doi.org/10.3390/cancers15164150 - 17 Aug 2023
Cited by 5 | Viewed by 2070
Abstract
Background: Diffuse large B-cell lymphoma (DLBCL) is a malignant lymphoid tumor disease that is characterized by heterogeneity, but current treatment does not benefit all patients, which highlights the need to identify oncogenic genes and appropriate drugs. G9a is a histone methyltransferase that catalyzes [...] Read more.
Background: Diffuse large B-cell lymphoma (DLBCL) is a malignant lymphoid tumor disease that is characterized by heterogeneity, but current treatment does not benefit all patients, which highlights the need to identify oncogenic genes and appropriate drugs. G9a is a histone methyltransferase that catalyzes histone H3 lysine 9 (H3K9) methylation to regulate gene function and expression in various cancers. Methods: TCGA and GTEx data were analyzed using the GEPIA2 platform. Cell viability under drug treatment was assessed using Alamar Blue reagent; the interaction between G9a and niclosamide was assessed using molecular docking analysis; mRNA and protein expression were quantified in DLBCL cell lines. Finally, G9a expression was quantified in 39 DLBCL patient samples. Results: The TCGA database analysis revealed higher G9a mRNA expression in DLBCL compared to normal tissues. Niclosamide inhibited DLBCL cell line proliferation in a time- and dose-dependent manner, reducing G9a expression and increasing p62, BECN1, and LC3 gene expression by autophagy pathway regulation. There was a correlation between G9a expression in DLBCL samples and clinical data, showing that advanced cancer stages exhibited a higher proportion of G9a-expressing cells. Conclusion: G9a overexpression is associated with tumor progression in DLBCL. Niclosamide effectively inhibits DLBCL growth by reducing G9a expression via the cellular autophagy pathway; therefore, G9a is a potential molecular target for the development of therapeutic strategies for DLBCL. Full article
(This article belongs to the Special Issue Autophagy–EMT Interrelations: At the Core of Tumor Transformation)
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Review

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31 pages, 9007 KiB  
Review
Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression
by Raffaele Strippoli, Reyhaneh Niayesh-Mehr, Maryam Adelipour, Arezoo Khosravi, Marco Cordani, Ali Zarrabi and Abdolamir Allameh
Cancers 2024, 16(4), 807; https://doi.org/10.3390/cancers16040807 - 16 Feb 2024
Cited by 8 | Viewed by 1867
Abstract
Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as [...] Read more.
Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as protein/DNA aggregates and abnormal organelles are degraded in specific lysosomes. In cancer, autophagy plays a controversial role, acting in different conditions as both a tumor suppressor and a tumor-promoting mechanism. Experimental evidence shows that deep interrelations exist between EMT and autophagy-related pathways. Although this interplay has already been analyzed in previous studies, understanding mechanisms and the translational implications of autophagy/EMT need further study. The role of autophagy in EMT is not limited to morphological changes, but activation of autophagy could be important to DNA repair/damage system, cell adhesion molecules, and cell proliferation and differentiation processes. Based on this, both autophagy and EMT and related pathways are now considered as targets for cancer therapy. In this review article, the contribution of autophagy to EMT and progression of cancer is discussed. This article also describes the multiple connections between EMT and autophagy and their implication in cancer treatment. Full article
(This article belongs to the Special Issue Autophagy–EMT Interrelations: At the Core of Tumor Transformation)
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48 pages, 7853 KiB  
Review
Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer
by Javad Alizadeh, Mahboubeh Kavoosi, Navjit Singh, Shahrokh Lorzadeh, Amir Ravandi, Biniam Kidane, Naseer Ahmed, Fatima Mraiche, Michael R. Mowat and Saeid Ghavami
Cancers 2023, 15(8), 2195; https://doi.org/10.3390/cancers15082195 - 7 Apr 2023
Cited by 23 | Viewed by 5209
Abstract
Metabolic changes are an important component of tumor cell progression. Tumor cells adapt to environmental stresses via changes to carbohydrate and lipid metabolism. Autophagy, a physiological process in mammalian cells that digests damaged organelles and misfolded proteins via lysosomal degradation, is closely associated [...] Read more.
Metabolic changes are an important component of tumor cell progression. Tumor cells adapt to environmental stresses via changes to carbohydrate and lipid metabolism. Autophagy, a physiological process in mammalian cells that digests damaged organelles and misfolded proteins via lysosomal degradation, is closely associated with metabolism in mammalian cells, acting as a meter of cellular ATP levels. In this review, we discuss the changes in glycolytic and lipid biosynthetic pathways in mammalian cells and their impact on carcinogenesis via the autophagy pathway. In addition, we discuss the impact of these metabolic pathways on autophagy in lung cancer. Full article
(This article belongs to the Special Issue Autophagy–EMT Interrelations: At the Core of Tumor Transformation)
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