Autophagy and Tumor Microenvironment

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 1820

Special Issue Editor


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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
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Special Issue Information

Dear Colleagues,

Autophagy is a conserved catabolic process, essential for the maintenance of cellular homeostasis. It exhibits a dual-sided role in cancer: it promotes clearance of transformed cells and inhibits tumorigenesis, while also sustaining cancer as a drug-resistance mechanism. Autophagy signaling in the tumor microenvironment (TME) during cancer growth and therapy is not adequately understood.

 The aims of this Special Issue are the following:

  • Highlight the role of autophagy signaling pathways to support cancer growth and progression in adaptation to the oxidative and hypoxic context of the TME;
  • Understand the role of autophagy in regulating the metabolic switch for generating sufficient levels of high-energy metabolites for cancer cell survival;
  • Clarify its critical role in modulating tumor-associated fibroblasts resulting in cytokine- and paracrine-signaling-mediated angiogenesis and invasion of pre-metastatic niches to secondary tumor sites;
  • Understand how autophagy promotes immune evasion to inhibit antitumor immunity;
  • Uncover the role of autophagy in the TME in maintaining and supporting the survival of cancer stem cells resulting in chemoresistance and therapy recurrence.

Understanding the molecular mechanisms underlying the multiple roles of autophagy is important for the development of autophagy modulators for autophagy-based cancer therapy.

Dr. Maria Condello
Guest Editor

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Keywords

  • autophagy
  • cancer growth
  • cancer therapy
  • chemoresistance
  • microenvironment

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Published Papers (1 paper)

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Research

15 pages, 10511 KiB  
Article
Advancing Lung Cancer Treatment with Combined c-Met Promoter-Driven Oncolytic Adenovirus and Rapamycin
by Shih-Yao Chen, Chung-Teng Wang, Tang-Hsiu Huang, Jeng-Liang Tsai, Hao-Tien Wang, Yi-Ting Yen, Yau-Lin Tseng, Chao-Liang Wu, Jia-Ming Chang and Ai-Li Shiau
Cells 2024, 13(18), 1597; https://doi.org/10.3390/cells13181597 - 23 Sep 2024
Cited by 1 | Viewed by 1415
Abstract
Lung cancer remains a formidable health challenge due to its high mortality and morbidity rates. Non-small cell lung cancer (NSCLC) constitutes approximately 85% of all lung cancer cases, with small cell lung cancer (SCLC) accounting for the remainder. Both NSCLC and SCLC cells [...] Read more.
Lung cancer remains a formidable health challenge due to its high mortality and morbidity rates. Non-small cell lung cancer (NSCLC) constitutes approximately 85% of all lung cancer cases, with small cell lung cancer (SCLC) accounting for the remainder. Both NSCLC and SCLC cells express receptor tyrosine kinases, which may be overexpressed or mutated in lung cancer, leading to increased activation. The c-Met receptor tyrosine kinase, crucial for cell transformation and tumor growth, invasion, and metastasis, became the focus of our study. We used an E1B55KD-deleted, replication-selective oncolytic adenovirus (Ad.What), driven by the c-Met promoter, targeting lung cancer cells with c-Met overexpression, thus sparing normal cells. Previous studies have shown the enhanced antitumor efficacy of oncolytic adenoviruses when combined with chemotherapeutic agents. We explored combining rapamycin, a selective mTOR inhibitor with promising clinical trial outcomes for various cancers, with Ad.What. This combination increased infectivity by augmenting the expression of coxsackievirus and adenovirus receptors and αV integrin on cancer cells and induced autophagy. Our findings suggest that combining a c-Met promoter-driven oncolytic adenovirus with rapamycin could be an effective lung cancer treatment strategy, offering a targeted approach to exploit lung cancer cells’ vulnerabilities, potentially marking a significant advancement in managing this deadly disease. Full article
(This article belongs to the Special Issue Autophagy and Tumor Microenvironment)
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