分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

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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