MiR-34c-3p suppresses the proliferation and invasion of non-small cell lung cancer (NSCLC) by inhibiting PAC1/MAPK pathway

被引:2
|
作者
Zhou, Yuan-Li [1 ,2 ]
Xu, You-Jun [4 ]
Qiao, Chuan-Wu [3 ]
机构
[1] Shandong Univ, Jinan Cent Hosp, Dept Prevent, Jinan 250013, Shangdong, Peoples R China
[2] Shandong Univ, Jinan Cent Hosp, Hlth Sect, Jinan 250013, Shangdong, Peoples R China
[3] Shandong Univ, Jinan Cent Hosp, Dept Care Pharm, Jinan 250013, Shangdong, Peoples R China
[4] Shandong Univ, Jinan Cent Hosp, Reviewing Off Hlth Care, Jinan 250013, Shangdong, Peoples R China
关键词
miRNA-34c-3p; invasion; PAC1/MAPK pathway; NSCLC; ONE BINDING-PROTEIN; PROSTATE-CANCER; TUMOR-GROWTH; P38; MAPK; K-RAS; EXPRESSION; METASTASIS; INDUCTION; APOPTOSIS; ACTIVATION;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs have become recognized as key players in the development of malignancy. They are a family of small non-coding RNAs (22 nt similar to 30 nt) that can negatively regulate the expression of cancer-related genes by sequence selective targeting of mRNAs, leading to either mRNA translational repression or degradation. Lung cancer is the leading cause of cancer-related death worldwide with a substantially low survival rate. In this study, we analyzed the expression profile of miR-34c-3p in non-small cell lung cancer (NSCLC) tissues and cell lines, as its participation in some other types of cancer has been shown by previous reports. We found that miR-34c-3p was downregulated both in NSCLC tissues and cell lines. Overexpression of miR-34c-3p suppressed cell proliferation and colony formation and also limited migration and invasion in A549 cells. Furthermore, our results also shown miR-34c-3p reduction was associated with increased PAC1 expression levels in which miR-34c-3p downregulated PAC1 expression by recognizing and binding to specific binding sites in PAC1 3'-UTR. Taken together, our study implicates important roles of miR-34c-3p in NSCLC pathogenesis and implicates its potential application in cancer therapy.
引用
收藏
页码:6312 / 6322
页数:11
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