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Antitumor Activity of Berberine by Activating Autophagy and Apoptosis in CAL-62 and BHT-101 Anaplastic Thyroid Carcinoma Cell Lines

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机构: [1]Hebei Med Univ, Key Lab Neural & Vasc Biol, Minist Educ, Shijiazhuang 050017, Peoples R China [2]Hebei Med Univ, Dept Pharmacol, Key Lab Pharmacol & Toxicol New Drugs, Shijiazhuang 050017, Peoples R China [3]Hebei Med Univ, Dept Otorhinolaryngol Head & Neck Surg, Hosp 4, Shijiazhuang 050011, Peoples R China
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关键词: anaplastic thyroid carcinoma berberine autophagy apoptosis PI3K AKT mTOR reactive oxygen species

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Introduction: Anaplastic thyroid carcinoma (ATC) is the most lethal thyroid carcinoma. Doxorubicin (DOX) is the only drug approved for anaplastic thyroid cancer treatment, but its clinical use is restricted due to irreversible tissue toxicity. Berberine (BER), an isoquinoline alkaloid extracted from Coptidis Rhizoma, has been proposed to have antitumor activity in many cancers. However, the underlying mechanisms by which BER regulates apoptosis and autophagy in ATC remain unclear. Thus, the present study aimed to assess the therapeutic effect of BER in human ATC cell lines CAL-62 and BHT-101 as well as the underlying mechanisms. In addition, we assessed the antitumor effects of a combination of BER and DOX in ATC cells. Methods: The cell viability of CAL-62 and BTH-101 with treatment of BER for different hours was measured by CCK-8 assay, and cell apoptosis was assessed by clone formation assay and flow cytometric analysis. The protein levels of apoptosis protein, autophagy-related proteins and PI3K/AKT/mTORpathway were determined Using Western blot. Autophagy in cells was observed with GFP-LC3 plasmid using confocal fluorescent microscopy. Flow cytometry was used to detect intracellular ROS. Results: The present results showed that BER significantly inhibited cell growth and induced apoptosis in ATC cells. BER treatment also significantly upregulated the expression of LC3B-II and increased the number of GFP-LC3 puncta in ATC cells. Inhibition of autophagy by 3-methyladenine (3-MA) suppressed BER-induced autophagic cell death. Moreover, BER induced the generation of reactive oxygen species (ROS). Mechanistically, we demonstrated that BER regulated the autophagy and apoptosis of human ATC cells through the PI3K/AKT/mTOR pathways. Furthermore, BER and DOX cooperated to promote apoptosis and autophagy in ATC cells. Conclusion: Taken together, the present findings indicated that BER induces apoptosis and autophagic cell death by activating ROS and regulating the PI3K/AKT/mTOR signaling pathway.

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出版当年[2023]版:
大类 | 2 区 医学
小类 | 2 区 药物化学 2 区 药学
最新[2025]版:
大类 | 2 区 医学
小类 | 2 区 药物化学 2 区 药学
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出版当年[2023]版:
Q1 CHEMISTRY, MEDICINAL Q1 PHARMACOLOGY & PHARMACY
最新[2024]版:
Q1 CHEMISTRY, MEDICINAL Q1 PHARMACOLOGY & PHARMACY

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第一作者机构: [1]Hebei Med Univ, Key Lab Neural & Vasc Biol, Minist Educ, Shijiazhuang 050017, Peoples R China [2]Hebei Med Univ, Dept Pharmacol, Key Lab Pharmacol & Toxicol New Drugs, Shijiazhuang 050017, Peoples R China
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通讯机构: [3]Hebei Med Univ, Dept Otorhinolaryngol Head & Neck Surg, Hosp 4, Shijiazhuang 050011, Peoples R China
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