Zhang Jing, Zhang Feiyan, Fan Jiye, Feng Bin
Pharmacy Department, Hebei Chemical and Pharmaceutical College, Shijiazhuang, Hebei 050026, People's Republic of China.
Department of Outpatient Operating Room, Heze Municipal Hospital, Heze City, Shandong Province, 274000, People's Republic of China.
Cancer Manag Res. 2021 Mar 18;13:2603-2612. doi: 10.2147/CMAR.S254348. eCollection 2021.
Gastric cancer is a kind of cancer with high mortality. TGIF1, as a transcription inhibitor, can inhibit the transcription of specific genes. The purpose of this study was to investigate the role of TGIF1 in gastric cancer by knocking down TGIF1.
The expression of TGIF1 was detected by qPCR and Western blotting; CCK8 assay, colony formation assay, transwell, and wound-healing assay were used to evaluate the proliferation, migration, and invasion of gastric cancer cells; cell apoptosis was analyzed by flow cytometry and Hoechst-PI double staining; cell cycle was detected by flow cytometry. Gelatinase experiment was performed to detect the expression level of MMP-2; apoptosis related proteins and AKT singling pathway were assessed by Western blotting.
Knockdown of TGIF1 inhibited the proliferation, migration, and invasion of gastric cancer cells and promoted apoptosis. TGIF1 knockdown down-regulated the expression levels of MMP-2, Bcl2, CyclinD1, and p-Akt, and up-regulated the expression levels of Bax and Caspase3. These data suggested that knockdown of TGIF1 inhibited the development of gastric cancer via AKT signaling pathway.
TGIF1 knockdown inhibited the proliferation, migration, and invasion and promoted apoptosis of gastric cancer cells via the AKT signaling pathway, suggesting that TGIF1 is considered a potential inhibitor in gastric cancer.
胃癌是一种死亡率很高的癌症。TGIF1作为一种转录抑制剂,能够抑制特定基因的转录。本研究的目的是通过敲低TGIF1来探究其在胃癌中的作用。
采用qPCR和蛋白质免疫印迹法检测TGIF1的表达;运用CCK8法、集落形成实验、Transwell实验和伤口愈合实验评估胃癌细胞的增殖、迁移和侵袭能力;通过流式细胞术和Hoechst-PI双染法分析细胞凋亡情况;利用流式细胞术检测细胞周期。进行明胶酶实验以检测MMP-2的表达水平;通过蛋白质免疫印迹法评估凋亡相关蛋白和AKT信号通路。
敲低TGIF1可抑制胃癌细胞的增殖、迁移和侵袭,并促进细胞凋亡。敲低TGIF1下调了MMP-2、Bcl2,、CyclinD1和p-Akt的表达水平,上调了Bax和Caspase3的表达水平。这些数据表明,敲低TGIF1通过AKT信号通路抑制胃癌的发展。
敲低TGIF1通过AKT信号通路抑制胃癌细胞的增殖、迁移和侵袭,并促进细胞凋亡,提示TGIF1可被视为胃癌的一种潜在抑制因子。