Baicalein Mediated FAK Protein Regulates PI3K/Akt Signaling Pathway to Inhibit Proliferation and Migration of Gastric Cancer HGC-27 Cells
10.13422/j.cnki.syfjx.20220622
- VernacularTitle:黄芩素介导FAK蛋白调控PI3K/Akt信号通路抑制胃癌HGC-27细胞增殖和迁移
- Author:
Dan QIAO
1
;
Sheng-jun ZHANG
1
;
Shi-yu WANG
1
;
Guang-yuan YAO
1
;
Ying-lan CAI
1
;
Li-yan CHEN
1
;
Ying-shi PIAO
1
Author Information
1. Cancer Research Center of Yanbian University，Key Laboratory of Pathobiology （Yanbian University）， State Ethnic Affairs Commission，Research and Innovation Group of Yanbian University，Yanji 133002，China
- Publication Type:Journal Article
- Keywords:
baicalein;
gastric cancer;
focal adhesion kinase （FAK）;
cell proliferation;
phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(7):73-80
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo study the possible molecular mechanism of baicalein （BAI）-mediated focal adhesion kinase （FAK） in the regulation of phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway to inhibit the proliferation and migration of gastric cancer HGC-27 cells. MethodThe gastric epithelial GES-1 cells and gastric cancer HGC-27 cells were respectively treated with BAI （0， 5， 15， 25， and 50 μmol·L-1） for 48 h， and then methyl thiazolyl tetrazolium （MTT） assay was adopted to detect effect of BAI on cell proliferation. Western blot （WB） was employed to detect the expression of FAK and the proteins related to epithelial-mesenchymal transition （EMT） and PI3K signaling pathway after intervention with different concentrations of BAI. The HGC-27 cells stably overexpressing FAK were constructed with lentivirus-mediated transfection technique， and the transfection of FAK was detected through WB and green fluorescent protein （GFP）. The cells were divided into empty vector （NC） group， BAI group， FAK overexpression group， and BAI-treated FAK overexpression group， and cell proliferation activity was detected by MTT assay. The colony formation and cell migration were observed via colony formation assay and Transwell migration assay， respectively. The expression of proteins involved in EMT and PI3K signaling pathways were detected by Western blot. ResultCompared with the NC group， BAI （15， 25 and 50 μmol·L-1） inhibited the proliferation of HGC-27 cells in a dose-dependent manner （P<0.05， P<0.01） while did not affect that of GES-1 cells. BAI （5， 15 and 25 μmol·L-1） down-regulated the expression level of p-FAK （P<0.05， P<0.01）. Compared with NC group， FAK overexpression group showed up-regulated expression level of FAK in HGC-27 cells. The HGC-27 cells in both NC group and FAK overexpression group had green fluorescence. Compared with NC group， BAI inhibited the growth， colony formation， and migration， while FAK overexpression promoted those of HGC-27 cells. The treatment of FAK overexpression group with BAI inhibited the enhancement of cell proliferation and migration （P<0.05）. WB showed that compared with NC group， BAI （15， 25 μmol·L-1） significantly up-regulated the expression of E-cadherin protein and down-regulated that of Vimentin， Snail， p-PI3K， and p-Akt protein in HGC-27 cells （P<0.05， P<0.01）. Compared with NC group， FAK overexpression group showed down-regulated expression of E-cadherin， up-regulated expression of p-FAK， Vimentin， and Snail， and increased ratios of p-FAK/FAK， p-PI3K/PI3K and p-Akt/Akt （P<0.05）. This phenomenon would be reversed after BAI treatment. ConclusionBAI can affect the proliferation and migration of gastric cancer HGC-27 cells by mediating FAK to regulate PI3K/Akt signaling pathway.
