参佛胃康促进胃癌BGC-823细胞凋亡及可能机制  

Shenfoweikang promotes the apoptosis of gastric cancer cell and its possible mechanism

作　　者：魏鹏飞 黄辉 陈明霞 徐鹏飞 任革 王敏 王英英 孙嘉璐 丁垚 周小燕 WEI Peng-fei;HUANG Hui;CHEN Ming-xia;XU Peng-fei;REN Ge;WANG Min;WANG Ying-ying;SUN Jia-lu;DING Yao;ZHOU Xiao-yan(Department of Radiotherapy,Shaanxi University of Traditional Chinese Medicine,Xianyang 712000,China;Department of Oncology,Affiliated Hospital,Shaanxi University of Traditional Chinese Medicine,Xianyang 712000,China;School of Medical Technology,Shaanxi University of Traditional Chinese Medicine,Xianyang 712000,China)

机构地区：[1]陕西中医药大学附属医院放疗科,陕西咸阳712000 [2]陕西中医药大学附属医院肿瘤二科,陕西咸阳712000 [3]陕西中医药大学医学技术学院,陕西咸阳712000

出　　处：《解剖科学进展》2022年第2期229-233,238,共6页Progress of Anatomical Sciences

基　　金：陕西省中医管理局中医药科研课题(JCPT004)。

摘　　要：目的 探讨参佛胃康对胃癌BGC-823细胞的作用及机制。方法 使用参佛胃康处理BGC-823细胞,应用Western blot检测其miR-495-3p的表达量,应用Annexin V染色检测细胞凋亡水平;梯度敲低miR-495-3p并用参佛胃康处理,检测BGC-823的凋亡情况。通过miRDB在线分析和荧光素酶报告系统分析miR-495-3p是否靶向血小板反应蛋白2(THBS2);在过表达或敲低miR-495-3p的情况下,检测THB2和PI3K/Akt通路核心蛋白的表达量,检测BGC-823的凋亡水平。结果 参佛胃康促进BGC-823胃癌细胞凋亡,上调miR-495-3p的表达量。梯度敲低miR-495-3p并用参佛胃康处理后,BGC-823的凋亡水平受到梯度抑制。miR-495-3p靶向THBS2的3’非编码区。过表达miR-495-3p后,THBS2及PI3K/Akt通路核心蛋白AKT和PI3的表达量均下降,促进BGC-823细胞凋亡。敲低miR-495-3p后,THBS2及PI3K/Akt通路核心蛋白AKT和PI3的表达量均上升,抑制BGC-823凋亡。过表达或敲低miR-495-3p的同时回补THBS的表达,PI3K/Akt通路核心蛋白的表达量以及BGC-823的凋亡水平均无显著差异。结论 参佛胃康促进BGC-823胃癌细胞凋亡,miR-495-3p降低THBS2的表达量,与降低PI3K/Akt通路活性相关。Objective To investigate the effect and potential mechanism of Shenfoweikang on gastric cancer cells. Methods Shenfoweikang was used to treat BGC-823, and the expression of miR-495-3p was determined by Western blot, and apoptosis were measured by Annexin V staining. miR-495-3p targeting Thrombospondin 2(THBS2) was analyzed by miRDB online analysis and photonase reporting system;the expression of core protein THB2 and PI3K/Akt pathway and BGC-823 apoptosis level were detected under the condition of overexpression or knockdown of miR-495-3p.Results Shenfoweikang increased the apoptosis level of BGC-823, and the expression level of miR-495-3p. The apoptosis level of BGC-823 was inhibited by gradient knockdown of miR-495-3p and Shenfoweikang. And also demonstrated that miR-495-3p targeted the 3’non-coding region of THBS2. Over-expressed miR-495-3p downregulated the expression levels of THBS2 and PI3K/Akt pathway core proteins AKT and PI3, and promoted BGC-823 apoptosis levels. Knockdown of miR-495-3p upregulated the expression levels of THBS2 and PI3K/Akt pathway core proteins AKT and PI3 increased, and inhibited BGC-823 apoptosis. However, there was no significant difference for the expression level of PI3K/Akt core protein and BGC-823 apoptosis level when miR-495-3p was overexpressed or inhibited while THBS expression was replenished.Conclusion Shenfoweikang promotes the apoptosis of gastric cancer cells, which is related to the decrease of PI3K/Akt pathway activity and the expression level of THBS2 via miR-495-3p.

关 键 词：参佛胃康 胃癌 miR-495-3p PI3K AKT 细胞凋亡 

分 类 号：R735.2[医药卫生—肿瘤]