Wan Yiyuan, Luo Hesheng, Yang Ming, Tian Xia, Peng Bo, Zhan Ting, Chen Xiaoli, Ding Yu, He Jinrong, Cheng Xueting, Huang Xiaodong, Zhang Yadong
Department of Gastroenterology, Wuhan Third Hospital, Tongren Hospital of Wuhan University, Wuhan 430060, China.
Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Mol Ther Oncolytics. 2020 Jul 31;18:432-442. doi: 10.1016/j.omto.2020.07.011. eCollection 2020 Sep 25.
Pancreatic cancer cells are characterized by high cell proliferation and low cell apoptosis, but the factors involved in these processes remain to be further studied. In this study, we report that miR-324-5p regulates the proliferation and apoptosis of pancreatic cancer cells through regulating the expression of Krüppel-like factor 3 (KLF3). In both pancreatic cancer tissues and cell lines, the levels of miR-324-5p are significantly increased. Inhibition of miR-324-5p represses cell proliferation but promotes cell apoptosis, whereas overexpression of miR-324-5p exerts the opposite effect. Furthermore, we identified KLF3, a factor regulating pancreatic cancer cell proliferation and apoptosis, as a new direct downstream target of miR-324-5p. Our results suggest that miR-324-5p plays an important role in pancreatic cancer cell proliferation and apoptosis via downregulating the expression of KLF3.
胰腺癌细胞的特征是高细胞增殖和低细胞凋亡，但参与这些过程的因素仍有待进一步研究。在本研究中，我们报道miR-324-5p通过调节Krüppel样因子3（KLF3）的表达来调节胰腺癌细胞的增殖和凋亡。在胰腺癌组织和细胞系中，miR-324-5p的水平均显著升高。抑制miR-324-5p可抑制细胞增殖但促进细胞凋亡，而miR-324-5p的过表达则产生相反的效果。此外，我们确定了调节胰腺癌细胞增殖和凋亡的因子KLF3是miR-324-5p的一个新的直接下游靶点。我们的结果表明，miR-324-5p通过下调KLF3的表达在胰腺癌细胞增殖和凋亡中发挥重要作用。
