长链非编码RNA BCAR4对胰腺癌细胞增殖和凋亡的影响及机制

目的:探讨长链非编码RNA BCAR4(LncRNA BCAR4)在胰腺癌细胞中的表达以及对胰腺癌细胞增殖和凋亡的影响。方法:用qRT-PCR检测胰腺癌细胞系(AsPC-1、HPAC、BxPC-3、Panc-1)和正常胰腺导管上皮细胞系HPDE6-C7中LncRNA BCAR4的表达。将胰腺癌AsPC-1细胞分别转染BCAR4 siRNA序列和阴性对照siRNA序列,以无转染的AsPC-1细胞为空白对照,用CCK-8和流式细胞术检测细胞的增殖和凋亡,Western blot检测细胞中mTOR与P70S6K及磷酸化mTOR(p-mTOR)与磷酸化P70S6K(p-P70S6K)蛋白的表达。结果:LncRNA BCAR4在各胰腺癌细胞系中的相对表达量均明显高于正常胰腺导管上皮细胞系HPDE6-C7(均P0.05);AsPC-1细胞转染BCAR4 siRNA后表现为增殖能力明显降低、凋亡率明显升高、p-mTOR及p-P70S6K蛋白相对表达量明显降低(均P0.05)。结论:LncRNA BCAR4在胰腺癌细胞中表达升高,LncRNA BCAR4的高表达可促进胰腺癌细胞增殖抑制凋亡,机制可能与LncRNA BCAR4上调mTOR/P70S6K通路的磷酸化水平有关。

Effect of long non-coding RNA BCAR4 on proliferation and apoptosis of pancreatic carcinoma cells and the mechanism

Objective: To investigate the expression of long non-coding RNA BCAR4 (LncRNA BCAR4) in pancreatic carcinoma cells and its effects on proliferation and apoptosis of pancreatic carcinoma cells. Methods: The expressions of LncRNA BCAR4 in different pancreatic carcinoma cell lines (AsPC-1, HPAC, BxPC-3 and Panc-1) and normal pancreatic duct epithelial cells HPDE6-C7 were determined by qRT-PCR method. The pancreatic carcinoma AsPC-1 cells were transfected with BCAR4 siRNA or crambled sequences, with untransfected AsPC-1 cells as blank control, and then the cell proliferation and apoptosis were measured by CCK-8 assay and flow cytometry, and the protein expression levels of p-mTOR and p-P70S6K as well as phosphorylated mTOR (p-mTOR) and phosphorylated P70S6K (p-P70S6K) were detected by Western blot analysis. Results: The relative expression levels of LncRNA BCAR4 in all studied pancreatic carcinoma cell lines were significantly higher than that in normal pancreatic duct epithelial HPDE6-C7 cells (all P<0.05). After BCAR4 siRNA transfection, AsPC-1 cells exhibited decreased proliferation, increased apoptosis rate and down-regulated p-mTOR and p-P70S6K expressions (all P<0.05). Conclusion: LncRNA BCAR4 expression is increased in pancreatic carcinoma cells. High LncRNA BCAR4 expression can promote proliferation and inhibit apoptosis of the pancreatic carcinoma cells, and the mechanism may be associated with its up-regulating phosphorylation level of mTOR/P70S6K pathway.