Zhang Lian, Lei Yunlong, Zhang Ying, Li Yi, Bu Youquan, Song Fangzhou, Zhang Chundong
Department of Biochemistry and Molecular Biology, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing, 400016, China.
Molecular Medicine and Cancer Research Center, Chongqing Medical University, 1 Yixueyuan Road, Yuzhong District, Chongqing, 400016, China.
Genes Dis. 2017 Dec 28;5(2):158-166. doi: 10.1016/j.gendis.2017.12.003. eCollection 2018 Jun.
Our previous studies have demonstrated that proline-rich protein 11 (PRR11) is a novel tumor-related gene and implicates in regulating the proliferation in lung cancer. However, its precise role in cell cycle progression remains unclear. Our recent evidences show that PRR11 silencing has an effect on autophagy in non-small-cell lung cancer (NSCLC) cells. Two human NSCLC cell lines, H1299 and A549 were transiently transfected with against PRR11 siRNA. The Cell Counting Kit-8 and plate clone formation assay showed that downregulation of PRR11 inhibited the cell proliferation associated with cell cycle related genes reduced. And our data suggested that PRR11 depletion expression enhanced the autophagosomes formation, followed with downregulation of P62 and upregulation of LC3-II protein. Furthermore, the immunoblotting results indicated that silencing of PRR11 inactivated the Akt/mTOR signaling pathway. Collectively, these results demonstrated PRR11 had an effective role in autophagy in NSCLC cells through Akt/mTOR autophagy signaling pathways. Therefore, it is helpful to clarify the function of PRR11 in tumorigenesis of NSCLC.
我们之前的研究表明，富含脯氨酸的蛋白11（PRR11）是一种新型肿瘤相关基因，参与调控肺癌细胞的增殖。然而，其在细胞周期进程中的具体作用仍不清楚。我们最近的证据表明，PRR11沉默对非小细胞肺癌（NSCLC）细胞的自噬有影响。使用针对PRR11的小干扰RNA（siRNA）瞬时转染两个人非小细胞肺癌细胞系H1299和A549。细胞计数试剂盒-8（CCK-8）和平板克隆形成试验表明，PRR11的下调抑制了细胞增殖，同时与细胞周期相关基因的表达降低有关。我们的数据表明，PRR11表达缺失增强了自噬体的形成，随后P62表达下调，微管相关蛋白1轻链3-II（LC3-II）蛋白表达上调。此外，免疫印迹结果表明，PRR11沉默使Akt/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路失活。总的来说，这些结果表明PRR11通过Akt/mTOR自噬信号通路在NSCLC细胞的自噬中发挥有效作用。因此，这有助于阐明PRR11在NSCLC肿瘤发生中的功能。
