Department of medical administration, Henan Provincial People's Hospital, Department of medical administration of Central China Fuwai Hospital, Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, 450003, Henan Province, China.
Gastroenterology department, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, Henan Province, China.
Biomed Pharmacother. 2019 Dec;120:109443. doi: 10.1016/j.biopha.2019.109443. Epub 2019 Sep 18.
To investigate the effect of rosmarinic acid (RosA) on hepatocellular carcinoma cell in vivo and in vitro and to explore its possible mechanism of anti-hepatocarcinoma.
The hepatocellular carcinoma cell line SMMC-7721 was treated with different concentrations of RosA (0, 20, 50, 100 μmol/L) to detect cell proliferation, cell cycle, apoptosis and invasion.PI3K pathway-specific activator IGF-1 was used to explore whether the mechanism for RosA action relates to PI3K/AKT signal pathway.Nude mice inoculated with SMMC-7721 cells were treated with different doses of RosA (0, 5, 10 and 20 mg/kg) to detect the tumor formation of cancer cells in vivo.
RosA significantly inhibited the proliferation of SMMC-7721 cells and induced G1 arrest and apoptosis in a dose-dependent manner. RosA might inhibit cell invasion by regulating epithelial-mesenchymal transition. Rescue experiments showed that IGF-1 could reverse the inhibition of PI3K/AKT/mTOR signal pathway by RosA and the effect on proliferation, apoptosis, cell cycle, invasion and EMT by IGF-1 in SMMC-7721 cells;RosA could inhibit tumor formation of SMMC-7721 cells in vivo.
RosA can inhibit the proliferation and invasion of hepatocellular carcinoma cell in vitro and inhibit tumour growth in vivo and the mechanism may relate to inhibiting the activation of PI3K/AKT signal pathway.
研究迷迭香酸（RosA）在体内和体外对肝癌细胞的影响，并探讨其抗肝癌的可能机制。
用不同浓度的 RosA（0、20、50、100μmol/L）处理肝癌细胞系 SMMC-7721，检测细胞增殖、细胞周期、凋亡和侵袭。用 PI3K 通路特异性激活剂 IGF-1 来探索 RosA 作用的机制是否与 PI3K/AKT 信号通路有关。用不同剂量的 RosA（0、5、10 和 20mg/kg）处理接种 SMMC-7721 细胞的裸鼠，检测体内癌细胞的肿瘤形成。
RosA 显著抑制 SMMC-7721 细胞的增殖，并呈剂量依赖性诱导 G1 期阻滞和凋亡。RosA 可能通过调节上皮间质转化来抑制细胞侵袭。挽救实验表明，IGF-1 可以逆转 RosA 对 PI3K/AKT/mTOR 信号通路的抑制作用，以及 IGF-1 对 SMMC-7721 细胞增殖、凋亡、细胞周期、侵袭和 EMT 的影响；RosA 可以抑制 SMMC-7721 细胞在体内的肿瘤形成。
RosA 可以抑制肝癌细胞在体外的增殖和侵袭，并抑制体内肿瘤生长，其机制可能与抑制 PI3K/AKT 信号通路的激活有关。
