MicroRNA-141-3p promoted the progression of nasopharyngeal carcinoma through targeting DLC1

被引:17
作者
Mu, J-W [1 ]
Zhou, X-Y [2 ]
Wang, Q-J [3 ]
Han, L-H [4 ]
Jiao, J-B [5 ]
机构
[1] Peoples Hosp Rizhao, ENT Dept, Rizhao, Peoples R China
[2] Rizhao Hosp TCM Rizhao, Dept Clin Lab, Rizhao, Peoples R China
[3] Peoples Hosp Zhangqiu Area, Dept Nephrol, Jinan, Peoples R China
[4] Peoples Hosp Zhangqiu Area, Dept Hlth Examinat, Jinan, Peoples R China
[5] Jining 1 Peoples Hosp, Dept Oncol, Jining, Peoples R China
关键词
MiR-141-3p; DLC1; Nasopharyngeal carcinoma; mTOR; CELL-PROLIFERATION; LOCAL RECURRENCE; INVASION; MIGRATION; METASTASIS; EXPRESSION; APOPTOSIS; BIOMARKER; GENE;
D O I
10.26355/eurrev_202011_23597
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
OBJECTIVE: Previous studies have shown that the function of miR-141 has tissue specificity. However, the role of miR-141-3p has not been reported in nasopharyngeal carcinoma (NPC). Therefore, this study explored the function of miR-141-3p in NPC. PATIENTS AND METHODS: MiR-141-3p expression in NPC tissues was examined via quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. Cell Counting Kit-8 (CCK-8) and transwell assays were used to explore the function of miR-141-3p. The relationship between miR-141-3p and DLC1 was verified by Dual-Luciferase assay. Protein expression was observed by immunocytochemical assay and Western blot analysis. RESULTS: Upregulation of miR-141-3p associated with poor prognosis was detected in NPC patients. Moreover, overexpression of miR-141-3p promoted cell proliferation, migration, and invasion in NPC cells. It was also found that miR-141-3p promoted EMT and activated the mTOR signaling pathway in NPC. Furthermore, DLC1 was indicated as a direct target of miR-141-3p and miR-141-3p negatively correlated with DLC1 expression in NPC. In particular, upregulation of DLC1 could impair the promoted effect of miR-141-3p in NPC. CONCLUSIONS: MiR-141-3p promotes the progression of NPC by targeting DLC1 and activating the mTOR pathway.
引用
收藏
页码:11105 / 11113
页数:9
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