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Objective <p>This research aimed to explore the anti-tumor mechanism of berberine (BBR) in papillary thyroid carcinoma (PTC) through the PINK1/Parkin pathway.</p> Methods <p>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.</p> Results <p>BBR (100 and 150&#xa0;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.</p> Conclusion <p>BBR significantly prevents TPC-1 cell proliferation and metastasis by activating the PINK1/Parkin pathway and promoting mitochondrial autophagy.</p>

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Regulation of PINK1/Parkin signaling pathway by berberine mediates mitochondrial autophagy to intervene in the proliferation and metastasis of thyroid cancer

  • 期刊论文

  • 发表日期：

    2026年2月10日

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  • Xiang Geng,
  • YangYang Sun,
  • JinJin Fu,
  • Liang Cao,
  • Yuan Li

摘要

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.