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Autophagy Induced by Metabolic Processes Leads to Solid Tumor Cell Metastatic Dormancy and Recurrence Publisher Pubmed



Ferdousmakan S1 ; Mansourian D2 ; Seyedi Asl FS3 ; Fathi Z3 ; Malekisheikhabadi F4 ; Afjadi MN5 ; Zalpoor H6, 7
Authors
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Authors Affiliations
  1. 1. Department of Pharmacy Practice, Nargund College of Pharmacy, Bangalore, 560085, India
  2. 2. Faculty of Pharmacy, Eastern Mediterranean University, Gazimagusa TRNC via Mersin 10, Mersin, Turkey
  3. 3. Medical School, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Hematology and Blood Banking, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
  5. 5. Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
  6. 6. Network of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran
  7. 7. Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

Source: Medical Oncology Published:2025


Abstract

A crucial cellular mechanism that has a complex impact on the biology of cancer, particularly in solid tumors, is autophagy. This review explores how metabolic processes trigger autophagy, which helps metastatic tumor cells go dormant and recur. During metastasis, tumor cells frequently encounter severe stressors, such as low oxygen levels and nutritional deprivation, which causes them to activate autophagy as a survival tactic. This process allows cancer stem cells (CSCs) to withstand severe conditions while also preserving their features. After years of dormancy, dormant disseminated tumor cells (DTCs) may reappear as aggressive metastatic cancers. The capacity of autophagy to promote resistance to treatments and avoid immune detection is intimately related to this phenomenon. According to recent research, autophagy promotes processes, such as the epithelial-to-mesenchymal transition (EMT) and helps build a pre-metastatic niche, which makes treatment strategies more challenging. Autophagy may be a promising therapeutic target because of its dual function as a tumor suppressor in early-stage cancer and a survival promoter in advanced stages. To effectively treat metastatic diseases, it is crucial to comprehend how metabolic processes interact with autophagy and affect tumor behavior. In order to find novel therapeutic approaches that can interfere with these processes and improve patient outcomes, this study highlights the critical need for additional investigation into the mechanisms by which autophagy controls tumor dormancy and recurrence. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.
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