Regulation of PINK1/Parkin signaling pathway by berberine mediates mitochondrial autophagy to intervene in the proliferation and metastasis of thyroid cancer
Geng Xiang, Sun YangYang, Fu JinJin, Cao Liang, Li Yuan
Journal:Molecular & Cellular Toxicology
IF:1.4
DOI:10.1007/s13273-026-00605-x
PMID:
Published:2026-02-10
research field:肿瘤学分子生物学药理学细胞生物学
Abstract
Objective This research aimed to explore the anti-tumor mechanism of berberine (BBR) in papillary thyroid carcinoma (PTC) through the PINK1/Parkin pathway. Methods TPC-1 and Nthy-ori3-1 cells were treated with different concentrations of BBR to determine the optimal dose. PINK1/Parkin signaling pathway was intervened in TPC-1 cells by transfection, followed by detection of mitochondrial superoxide levels (using MitoSOX), mitochondrial membrane potential (MMP), cell proliferation, invasion, migration, and related protein expression. Results BBR (100 and 150 μM) inhibited TPC-1 cell proliferation, invasion, and migration. BBR reduced mitochondrial autophagy as evidenced by higher mitochondrial superoxide production, lower MMP, decreased p62, and increased PINK1, Parkin, and ATG5. PINK1 knockdown promoted TPC-1 cell proliferation and metastasis by blocking mitochondrial autophagy. BBR inhibited TPC-1 proliferation and metastasis by activating the PINK1/Parkin pathway. Conclusion BBR significantly prevents TPC-1 cell proliferation and metastasis by activating the PINK1/Parkin pathway and promoting mitochondrial autophagy.
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