ArticleFrontiers in oncology2026
TGFBR3 regulates the expression of FATP2-ACSL1 axis related proteins and accompanies changes in the migration and invasion ability of lung cancer cells.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Abnormal lipid metabolism promotes lung cancer progression. This study explores how TGFBR3 regulates fatty-acid-metabolism-related protein expression via the FATP2-ACSL1 axis to suppress lung cancer invasion and metastasis, and preliminarily assesses the potential clinical value of TGFBR3 and FATP2. Methods: Serum samples were collected from 30 healthy individuals and 170 newly diagnosed lung cancer patients for lipid profiling. Network pharmacology, Mendelian randomization, molecular docking, co-immunoprecipitation (Co-IP) and GST-Pull down assay were used to validate the TGFBR3-FATP2 interaction. Stable cell lines were established to assess function and mechanism via CCK-8, wound healing, Transwell, and Western blotting. Serum levels of soluble TGFBR3 (sTGFBR3) and FATP2 were measured by ELISA. Results: Serum CHOL, HDL-C, and LDL-C were significantly decreased in lung cancer patients ( Conclusions: TGFBR3 interacts with FATP2 and is associated with the regulation of migration and invasion in lung cancer cells, potentially involving the FATP2-ACSL1 axis. Additionally, serum levels of sTGFBR3 and FATP2 were identified as potential candidate biomarkers for lung cancer, warranting further validation in independent cohorts migration.
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