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Carnosol Inhibits the Proliferation, Migration, and Invasion of Hepatocellular Carcinoma Cells in vitro by Regulating the AMPK Signaling Pathway

癌症研究 活力测定 细胞生长 细胞凋亡 肝细胞癌 信号转导 生物 医学 药理学 细胞生物学 生物化学
作者
Shuang Kong,Wenchang Xiao,Tengfei Ma,Yun Chen,Hongjie Shi,Jun Tu,Jiahua Zou,Meng Zhang
出处
期刊:Anti-cancer Agents in Medicinal Chemistry [Bentham Science]
卷期号:23
标识
DOI:10.2174/1871520623666230418093254
摘要

Hepatocellular carcinoma (HCC) is one of the most malignant cancers in the world, and its 5- year survival rate is low. At present, for advanced primary liver cancer, the clinical treatment often adopts the systemic method, but there is no effective targeted treatment. The average survival time of patients with liver cancer after drug treatment is only 3-5 months. Therefore, it is of great clinical significance to find new and effective drugs for the treatment of HCC. Carnosol (CA) is a bioactive diterpene compound present in Lamiaceae spp., which has been demonstrated to have antioxidant, anti-inflammatory, and anticancer properties.In this study, we aimed to reveal the effect of carnosol on HCC and provide new possibilities for the drug therapy of HCC.The objective of this study is to observe the effect of carnosol on the tumor phenotype and signaling pathway of HCC cells.We treated two different human HCC cells, HepG2 and Huh7, with carnosol. The cells were analyzed using the CCK-8 assay for viability and proliferation. The cell migration and invasion were detected by Transwell assay. The molecular markers of cell proliferation, apoptosis, migration, invasion, and signaling pathways were detected by RTPCR and WB. In addition, we performed rescue experiments with inhibitors to verify the affected signaling pathway.The results showed that carnosol could significantly inhibit HCC cell viability, effort, colony formation, migration, and invasion. Moreover, Carnosol promoted the apoptosis of HCC cells. Mechanically, carnosol activated the AMPK-p53 pathway.To conclude, our study demonstrated that carnosol could inhibit proliferation, migration, invasion, and promote apoptosis via activating AMPK-p53 in HCC cells.

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