KLF8基因敲低可引发人胰腺癌细胞的生长抑制并诱导细胞周期阻滞。
KLF8 knockdown triggered growth inhibition and induced cell phase arrest in human pancreatic cancer cells.
作者信息
Yi Xiaoping, Li Yixiong, Zai Hongyan, Long Xueying, Li Wenzheng
机构信息
Department of Radiology, Xiangya Hospital, Central South University, Hunan 410008, PR China.
Department of General Surgery, Xiangya Hospital, Central South University, Hunan 410008, PR China.
出版信息
Gene. 2016 Jul 1;585(1):22-27. doi: 10.1016/j.gene.2016.03.025. Epub 2016 Mar 16.
BACKGROUND
The transcription factor Krüppel-like factor 8 (KLF8) plays an important role in tumor development and growth, but its role in pancreatic cancer (PC) is not clear.
METHODS
KLF8 expression in human PC cell lines and tumor tissues was measured by quantitative real-time polymerase chain reaction and Western blot analyses. The effects of lentivirus mediated knockdown of KLF8 on proliferation and growth in Panc-1 pancreatic cancer cells were examined.
RESULTS
KLF8 was overexpressed in 5 pancreatic cancer cell lines and in samples from patients with PC. In Panc-1 cells, KLF8 knockdown inhibited cell proliferation, tumorigenicity, and induced G2/M phase arrest. KLF8 knockdown suppressed PC tumor growth in nude mice model. Western blot analysis showed that KLF8 knockdown in Panc-1 cells down-regulated the expression of CDK1/CDC2, cyclin B1, and cyclin D1 and up-regulated the expression of p21, and p27.
CONCLUSIONS
Overexpression of KLF8 may contribute to the progression of pancreatic cancer, and downregulation of KLF8 expression by lentivirus-delivered shRNA is a novel therapeutic approach for PC.
背景
转录因子Krüppel样因子8（KLF8）在肿瘤发生和生长中起重要作用，但其在胰腺癌（PC）中的作用尚不清楚。
方法
通过定量实时聚合酶链反应和蛋白质免疫印迹分析检测人胰腺癌细胞系和肿瘤组织中KLF8的表达。研究慢病毒介导的KLF8敲低对Panc-1胰腺癌细胞增殖和生长的影响。
结果
KLF8在5种胰腺癌细胞系和胰腺癌患者样本中过表达。在Panc-1细胞中，KLF8敲低抑制细胞增殖、致瘤性并诱导G2/M期阻滞。KLF8敲低抑制裸鼠模型中的胰腺癌肿瘤生长。蛋白质免疫印迹分析表明，Panc-1细胞中KLF8敲低下调CDK1/CDC2、细胞周期蛋白B1和细胞周期蛋白D1的表达，并上调p21和p27的表达。
结论
KLF8的过表达可能促进胰腺癌的进展，通过慢病毒递送的短发夹RNA下调KLF8表达是一种新的胰腺癌治疗方法。
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