RETRACTED: MicroRNA-146-5p promotes proliferation, migration and invasion in lung cancer cells by targeting claudin-12 (Retracted Article)

被引:18
|
作者
Sun, Xianghong [1 ]
Cui, Shichao [2 ]
Fu, Xiaofeng [3 ]
Liu, Chuan [4 ]
Wang, Zhi [5 ]
Liu, Yuanwei [6 ]
机构
[1] Qingdao Univ, Dept Outpatient Tumor, Affiliated Hosp, West Coast Branch, Qingdao, Shandong, Peoples R China
[2] Qingdao Univ, Dept Resp Med, Affiliated Hosp, West Coast Branch, Qingdao, Shandong, Peoples R China
[3] Qingdao Univ, Dept Outpatient, Affiliated Hosp, West Coast Branch, Qingdao, Shandong, Peoples R China
[4] Qingdao West Coast New Dist 2 Peoples Hosp, Dept Surg, Qingdao, Shandong, Peoples R China
[5] Qingdao Univ, Dept Pharm, Affiliated Hosp, Shinan Branch, Qingdao, Shandong, Peoples R China
[6] Qingdao Univ, Dept Canc Comprehens Therapy, Affiliated Hosp, West Coast Branch, 1677 Wutaishan Rd, Qingdao 266000, Shandong, Peoples R China
关键词
miR-146-5p; lung cancer; cisplatin; claudin-12; wnt/beta-catenin; PI3K/AKT/MAPK signaling pathways; EXPRESSION; ASSOCIATION; METASTASIS; PROFILES; DELIVERY; RNAS;
D O I
10.3233/CBM-182374
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs (miRNAs) have been regarded as important regulators in different pathological processes of cells. Abnormal expression of miRNAs is frequently associated with cell proliferation, metastasis and apoptosis in various cancers. This study aimed to explore the effect of miR-146-5p on cell growth, metastasis and its mechanism in lung cancer cells. The expressions of miR-146-5p and claudin-12 in A549 and WI-38 cells were altered by transient transfection. Cisplatin was used to develop cells for regulation of cisplatin sensitivity. Cell viability, migration, invasion, and apoptosis were analyzed by CCK-8, Transwell and flow cytometry assays. The protein expressions of Wnt/beta-catenin and PI3K/AKT/MAPK pathway-related factors were detected. miR-146-5p suppression inhibited cell viability, migration and invasion but promoted apoptosis in A549 cells. Moreover, overexpression of miR-146-5p reduced the sensitivity of A549 cells and WI-38 cells to cisplatin. In addition, claudin-12 was a direct target of miR-146-5p and was negatively regulated by miR-146-5p. Claudin-12 silence significantly reversed miR-146-5p suppression-mediated anti-tumor effects in A549 cells. Furthermore, miR-146-5p overexpression activated Wnt/beta-catenin and PI3K/AKT/MAPK signal pathways via down-regulation of claudin-12. The results indicated that miR-146-5p promoted cell viability, migration and invasion, inhibited apoptosis and activated Wnt/beta-catenin and PI3K/AKT/MAPK signal pathways by regulating claudin-12 expression in lung cancer cells.
引用
收藏
页码:89 / 99
页数:11
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