Role of Autophagy in the Interactions between the Tumor and the Microenvironment

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

Deadline for manuscript submissions: closed (20 October 2022) | Viewed by 7413

Special Issue Editor


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Guest Editor
CEA/DRF/Institut Joliot, Université Côte d’Azur, UMR E4320 TIRO-MATOs, 06107 Nice CEDEX 2, France
Interests: autophagy; bone tissue; osteosarcoma; cancer stem cells; microenvironment

Special Issue Information

Dear Colleagues,

Autophagy is the major cellular process used for the degradation and recycling of damaged macromolecules and organelles. In addition to its constitutive role in cellular quality control, autophagy is stimulated in response to stress in order to promote survival.

In cancer, while autophagy exerts an inhibitory role in the early stages of tumor initiation, this process is also described to support the survival and growth of established tumors. Further to these known roles, autophagy recently emerged as an active contributor in the crosstalk between tumor and stromal cells. Tumor cell autophagy can modify the microenvironment through several pathways, including degradation, secretion, and signaling, leading to the inhibition of immune cell recruitment and activity, and resulting in tumor progression. Conversely, autophagy in stromal cells can feed the tumor, stimulate tumor growth, and favor the creation of a permissive immune microenvironment.

In this Special Issue on the “Role of Autophagy in the Interactions between the Tumor and the Microenvironment”, authors are invited to contribute through original or review articles to highlight this new role of autophagy. 

Dr. Valérie Pierrefite-Carle
Guest Editor

Manuscript Submission Information

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Keywords

  • autophagy
  • tumor
  • microenvironment
  • stromal cells
  • immune cells

Published Papers (2 papers)

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Review

18 pages, 1653 KiB  
Review
Secretory Autophagy Forges a Therapy Resistant Microenvironment in Melanoma
by Silvina Odete Bustos, Nathalia Leal Santos, Roger Chammas and Luciana Nogueira de Sousa Andrade
Cancers 2022, 14(1), 234; https://doi.org/10.3390/cancers14010234 - 04 Jan 2022
Cited by 7 | Viewed by 3757
Abstract
Melanoma is the most aggressive skin cancer characterized by high mutational burden and large heterogeneity. Cancer cells are surrounded by a complex environment, critical to tumor establishment and progression. Thus, tumor-associated stromal components can sustain tumor demands or impair cancer cell progression. One [...] Read more.
Melanoma is the most aggressive skin cancer characterized by high mutational burden and large heterogeneity. Cancer cells are surrounded by a complex environment, critical to tumor establishment and progression. Thus, tumor-associated stromal components can sustain tumor demands or impair cancer cell progression. One way to manage such processes is through the regulation of autophagy, both in stromal and tumor cells. Autophagy is a catabolic mechanism that provides nutrients and energy, and it eliminates damaged organelles by degradation and recycling of cellular elements. Besides this primary function, autophagy plays multiple roles in the tumor microenvironment capable of affecting cell fate. Evidence demonstrates the existence of novel branches in the autophagy system related to cytoplasmic constituent’s secretion. Hence, autophagy-dependent secretion assembles a tangled network of signaling that potentially contributes to metabolism reprogramming, immune regulation, and tumor progression. Here, we summarize the current awareness regarding secretory autophagy and the intersection with exosome biogenesis and release in melanoma and their role in tumor resistance. In addition, we present and discuss data from public databases concerning autophagy and exosome-related genes as important mediators of melanoma behavior. Finally, we will present the main challenges in the field and strategies to translate most of the pre-clinical findings to clinical practice. Full article
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18 pages, 1735 KiB  
Review
Autophagy and ncRNAs: Dangerous Liaisons in the Crosstalk between the Tumor and Its Microenvironment
by Gracie Wee Ling Eng, Yilong Zheng, Dominic Wei Ting Yap, Andrea York Tiang Teo and Jit Kong Cheong
Cancers 2022, 14(1), 20; https://doi.org/10.3390/cancers14010020 - 21 Dec 2021
Cited by 5 | Viewed by 2966
Abstract
Autophagy is a fundamental cellular homeostasis mechanism known to play multifaceted roles in the natural history of cancers over time. It has recently been shown that autophagy also mediates the crosstalk between the tumor and its microenvironment by promoting the export of molecular [...] Read more.
Autophagy is a fundamental cellular homeostasis mechanism known to play multifaceted roles in the natural history of cancers over time. It has recently been shown that autophagy also mediates the crosstalk between the tumor and its microenvironment by promoting the export of molecular payloads such as non-coding RNA (ncRNAs) via LC3-dependent Extracellular Vesicle loading and secretion (LDELS). In turn, the dynamic exchange of exosomal ncRNAs regulate autophagic responses in the recipient cells within the tumor microenvironment (TME), for both tumor and stromal cells. Autophagy-dependent phenotypic changes in the recipient cells further enhance tumor growth and metastasis, through diverse biological processes, including nutrient supplementation, immune evasion, angiogenesis, and therapeutic resistance. In this review, we discuss how the feedforward autophagy-ncRNA axis orchestrates vital communications between various cell types within the TME ecosystem to promote cancer progression. Full article
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