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黄芩苷通过下调Akt/mTOR信号通路诱导肺癌细胞凋亡并抑制其细胞周期进程。

Baicalin Induces Apoptosis and Suppresses the Cell Cycle Progression of Lung Cancer Cells Through Downregulating Akt/mTOR Signaling Pathway.

作者信息

Sui Xinbing, Han Xuemeng, Chen Peng, Wu Qibiao, Feng Jiao, Duan Ting, Chen Xiaying, Pan Ting, Yan Lili, Jin Ting, Xiang Yu, Gao Quan, Wen Chengyong, Ma Weirui, Liu Wencheng, Zhang Ruonan, Chen Bi, Zhang Mingming, Yang Zuyi, Kong Na, Xie Tian, Ding Xia

机构信息

School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.

Department of Medical Oncology, School of Medicine, The Affiliated Hospital of Hangzhou Normal University, College of Pharmacy, Hangzhou Normal University, Hangzhou, China.

出版信息

Front Mol Biosci. 2021 Jan 28;7:602282. doi: 10.3389/fmolb.2020.602282. eCollection 2020.

Abstract

Baicalin, as a natural active ingredient extracted and isolated from the traditional Chinese medicine Georgi., has been potentially used in various areas for its antioxidative, antitumor, anti-inflammatory, and anti-proliferative activities. Although several studies have reported the antitumor effects of baicalin against various cancer types, its beneficial effects on lung cancer have not yet been elucidated. Therefore, the therapeutic effects and molecular mechanisms of baicalin on lung cancer cell lines H1299 and H1650 were investigated. Here, the results of its antitumor activity were shown. We found that Akt/mTOR pathway inhibition was the essential determinant in baicalin-induced cell cycle arrest. Furthermore, when the Akt Agonist SC79 or Akt plasmid transfection was performed, the antitumor effect of baicalin was significantly abrogated in both H1299 and H1650 cells. In conclusion, we found that baicalin exerted its antitumor activity mainly by inducing Akt-dependent cell cycle arrest and promoting apoptosis, which show great potential for developing a new drug for lung cancer treatment.

摘要

黄芩苷是从传统中药黄芩中提取分离出的一种天然活性成分,因其具有抗氧化、抗肿瘤、抗炎和抗增殖活性,已在多个领域得到潜在应用。尽管多项研究报道了黄芩苷对多种癌症类型的抗肿瘤作用,但其对肺癌的有益作用尚未阐明。因此,研究了黄芩苷对肺癌细胞系H1299和H1650的治疗效果及分子机制。在此展示了其抗肿瘤活性的结果。我们发现抑制Akt/mTOR通路是黄芩苷诱导细胞周期停滞的关键决定因素。此外,当进行Akt激动剂SC79或Akt质粒转染时,黄芩苷在H1299和H1650细胞中的抗肿瘤作用均被显著消除。总之,我们发现黄芩苷主要通过诱导Akt依赖的细胞周期停滞和促进凋亡发挥其抗肿瘤活性,这为开发治疗肺癌的新药显示出巨大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a957/7876332/366156c16699/fmolb-07-602282-g001.jpg

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