ArticleJournal of translational medicine2025
PDGFR-β/Cav1-induced autophagy via mTOR/FIP200/ATG13 activation in cancer-associated fibroblasts promotes the malignant progression of breast cancer.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Epigallocatechin gallate is associated with PDGFRB downregulation and altered PI3K-AKT signaling in gastric cancer.Translational cancer research · 2026Article
- Radiation-activated astrocytes promote tumor progression through CXCL12 secretion and induce resistance to anti-PD-1 immunotherapy.Translational cancer research · 2026Article
- Qinggan Jianpi formula attenuates atherosclerosis by suppressing macrophage lactate transport to activate repair genes via H3K18 lactylation.Chinese medicine · 2026Article
- PHGDH knockdown activates autophagic flux to suppress migration and invasion of gastric cancer cells.Translational cancer research · 2026Article
- Lactate-lactylation in tumor angiogenesis and progression: mechanisms, biomarker potential, and therapeutic implications.Biomarker research · 2026Review
- The central role of EMT in tumor progression: mechanistic drivers, biomarker discovery, and therapeutic horizons.Frontiers in pharmacology · 2026Review
- Cancer-Associated Fibroblasts: Clinical Applications in Imaging and Therapy.Tomography (Ann Arbor, Mich.) · 2025Review
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- Mitophagy in gastrointestinal tumors: mechanisms and new targets for immunotherapy.Frontiers in oncology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundBreast cancer incidence rates have been increasing globally. Cancer-associated fibroblasts (CAFs), key stromal components of the tumor microenvironment (TME), play crucial roles in tumor growth by dynamically interacting with cancer cells. Autophagy has been extensively studied in multiple stages of the metastatic cascade. However, the roles of two key membrane proteins, platelet-derived growth factor receptor-β (PDGFR-β) and caveolin-1 (Cav-1), in regulating autophagy in CAFs and their effects on cancer cell invasion and migration remain unclear.
methodsThe association between PDGFR-β expression and clinical features in breast cancer patients was analyzed using TCGA databases. PDGFR-β was either overexpressed or pharmacologically inhibited in cancer cells. Autophagy-related markers and signaling proteins were analyzed by Western blot and RT-qPCR, while lactate secretion and ROS levels were quantified. Breast cancer cell migration and invasion were evaluated through wound healing and transwell assays, and PDGFR-β/Cav1 interactions were verified by immunofluorescence and co-immunoprecipitation (Co-IP). A breast cancer mouse model was employed to assess tumor progression and autophagy modulation in vivo.
resultsThe study demonstrated that PDGFR-β promotes autophagy in CAFs through the mTOR/FIP200/ATG13 signaling. PDGFR-β/Cav-1 enhanced glycolysis in CAFs via autophagy-mediated metabolic reprogramming, resulting in increased lactate export that promoted breast cancer cell growth. Furthermore, CAFs autophagy regulated breast cancer cell invasion and migration via the HIF-1α/MCT4/MCT1 signaling pathway. These findings reveal that PDGFR-β/Cav-1-mediated autophagy in CAFs enhances breast cancer cell invasion, migration, and epithelial-mesenchymal transition (EMT), collectively highlighting the crucial role of CAFs autophagy in facilitating breast cancer progression.
conclusionsThe study elucidates the mechanism by which PDGFR-β/Cav-1 promotes breast cancer progression through autophagy regulation in CAFs, These findings provide a theoretical basis for potential therapeutic method for treating breast cancer.
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