ArticleApoptosis : an international journal on programmed cell death2023
Cancer-associated fibroblasts promote malignant phenotypes of prostate cancer cells via autophagy : Cancer-associated fibroblasts promote prostate cancer development.
Article in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 21 citations in OpenAlex.
- 18 β-Glycyrrhetinic Acid Inhibits Malignant Progression of Prostate Cancer via Regulation of Autophagy and EMT Induced by PTEN/PI3K/mTOR Pathway.Clinical and experimental pharmacology & physiology · 2026Article
- Beyond the primary site: Molecular insights and clinical implications of cancer metastatic overlap between lung and urological organ cancers (Review).Molecular medicine reports · 2026Review
- DEC1 Deficiency Attenuates Breast Cancer-Induced Osteolytic Destruction by Suppression of Cancer-Associated Fibroblast Differentiation.Cancer medicine · 2026Article
- Investigating autophagy and miRNAs as therapeutic targets in leukemia.Discover oncology · 2026Review
- Cancer-Associated Fibroblasts in Prostate Cancer: Unraveling Mechanisms and Therapeutic Implications.Oncology research · 2026Review
- Death never dies: increasing impact of programmed cell death.Apoptosis : an international journal on programmed cell death · 2025Article
- Targeting the tumor microenvironment, a new therapeutic approach for prostate cancer.Prostate cancer and prostatic diseases · 2025Review
- Amlodipine, an L-type Ca2+ channel inhibitor, regulates release of extracellular vesicles from tumor cells.Carcinogenesis · 2025Article
- The role of cancer-associated fibroblasts in the tumour microenvironment of urinary system.Clinical and translational medicine · 2025Review
- A cellular danse macabre: the choreography of programmed cell death.Apoptosis : an international journal on programmed cell death · 2025Article
- NGR-Modified CAF-Derived exos Targeting Tumor Vasculature to Induce Ferroptosis and Overcome Chemoresistance in Osteosarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role and mechanisms of exosome microRNA in regulating metastasis within the tumor microenvironment of prostate cancer.Frontiers in oncology · 2025Review
- Application of Original Prostate Cancer Progression Model Interacting with Fibroblasts in Preclinical Research.Journal of clinical medicine · 2024Review
- Prostate cancer microenvironment: multidimensional regulation of immune cells, vascular system, stromal cells, and microbiota.Molecular cancer · 2024Review
- Targeting the autophagy-miRNA axis in prostate cancer: toward novel diagnostic and therapeutic strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Construction and validation of a ubiquitination-related prognostic risk score signature in breast cancer.Heliyon · 2024Article
- Crosstalk between cancer-associated fibroblasts and regulated cell death in tumors: insights into apoptosis, autophagy, ferroptosis, and pyroptosis.Cell death discovery · 2024Review
- The Mechanism by Which Hedgehog Interacting Protein (HHIP) in Cancer-Associated Fibroblasts Regulate the Secretion of Inflammatory Factors Through the JAK1/STAT3 Pathway Affecting Prostate Cancer Stemness.Journal of inflammation research · 2024Article
- Molecular Targeted Therapies in Metastatic Prostate Cancer: Recent Advances and Future Challenges.Cancers · 2023Review
- New insights into molecular signaling pathways and current advancements in prostate cancer diagnostics & therapeutics.Frontiers in oncology · 2023Review
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Dysregulation of autophagy in cancer-associated fibroblasts (CAFs) has been demonstrated to play a role in malignant phenotypes of human tumors. We intended to investigate the function of CAFs autophagy in prostate cancer (PCa). Firstly, CAFs and normal fibroblasts (NFs) were isolated from cancerous and adjacent normal tissues of PCa patients, for the following experimental preparation. In comparison with NFs, CAFs expressed higher levels of the myofibroblast marker ?-smooth muscle actin (?-SMA) and the mesenchymal marker Vimentin. Besides, CAFs possessed a higher autophagic level than NFs. As for malignant phenotypes, PCa cells co-cultured with CAFs-CM showed greater proliferation, migration and invasion capabilities, while these outcomes were obviously abolished by autophagy inhibition with 3-Methyladenine (3-MA). Moreover, silencing of ATG5 in CAFs inhibited fibroblasts autophagic level and suppressed malignant phenotypes of PCa cells, while ATG5 overexpression in NFs exerted opposite effects. Depletion of ATG5 in CAFs inhibited the xenograft tumor growth and lung metastasis of PCa cells. Taken together, our data demonstrated the promotive effect of CAFs on PCa malignant phenotypes through ATG5-dependent autophagy, suggesting a novel mechanism for PCa progression.
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