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Cells
Special Issues
Autophagy and Tumor Microenvironment
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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 2106

Special Issue Editor

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 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

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. Cells 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 2700 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
  • cancer growth
  • cancer therapy
  • chemoresistance
  • microenvironment

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Published Papers (2 papers)

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Research

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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 1459
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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Review

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27 pages, 1400 KiB  
Review
Perspectives of Targeting Autophagy as an Adjuvant to Anti-PD-1/PD-L1 Therapy for Colorectal Cancer Treatment
by Nasrah ALKhemeiri, Sahar Eljack and Maha Mohamed Saber-Ayad
Cells 2025, 14(10), 745; https://doi.org/10.3390/cells14100745 - 20 May 2025
Viewed by 205
Abstract
Colorectal cancer (CRC) is the third most common cancer in the world, with increasing incidence and mortality rates. Standard conventional treatments for CRC are surgery, chemotherapy, and radiotherapy. Recently, immunotherapy has been introduced as a promising alternative to CRC treatment that utilizes patients’ [...] Read more.
Colorectal cancer (CRC) is the third most common cancer in the world, with increasing incidence and mortality rates. Standard conventional treatments for CRC are surgery, chemotherapy, and radiotherapy. Recently, immunotherapy has been introduced as a promising alternative to CRC treatment that utilizes patients’ immune system to combat cancer cells. The beneficial effect of immune checkpoint inhibitors, specifically anti-PD-1/ PD-L1, has been ascribed to the abundance of DNA replication errors that result in the formation of neoantigens. Such neoantigens serve as distinct flags that amplify the immune response when checkpoint inhibitors (ICIs) are administered. DNA replication errors in CRC patients are expressed as two statuses: the first is the deficient mismatch repair (MSI-H/dMMR) with a higher overall immune response and survival rate than the second status of patients with proficient mismatch repair (MSS/pMMR). There is a limitation to using anti-PD-1/PD-L1 as it is only confined to MSI-H/dMMR, where there is an abundance of T-cell inhibitory ligands (PD-L1). This calls for investigating new therapeutic interventions to widen the scope of ICIs’ role in the treatment of CRC. Autophagy modulation provides a good example. Autophagy is a cellular process that plays a crucial role in maintaining cellular homeostasis and has been studied for its impact on tumor development, progression, and response to treatment. In this review, we aim to highlight autophagy as a potential determinant in tumor immune response and to study the impact of autophagy on the tumor immune microenvironment. Moreover, we aim to investigate the value of a combination of anti-PD-1/PD-L1 agents with autophagy modulators as an adjuvant therapeutic approach for CRC treatment. Full article
(This article belongs to the Special Issue Autophagy and Tumor Microenvironment)
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