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miR‐143 inhibits proliferation and metastasis of nasopharyngeal carcinoma cells via targeting FMNL1 based on clinical and radiologic findings
Author(s) -
Cui Fusheng,
Ji Yuqing,
Wang Man,
Gao Fengxiao,
Li Yongcai,
Li Xueshen
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28709
Subject(s) - nasopharyngeal carcinoma , gene knockdown , ectopic expression , western blot , microrna , cell growth , cancer research , metastasis , biology , blot , cell culture , pathology , gene , medicine , cancer , genetics , radiation therapy
Abstract Mounting evidence has reported that microRNA‐143 (miR‐143) is involved in the development of multiple cancers. To investigate the underlying mechanisms of miR‐143 regulating proliferation and metastasis in nasopharyngeal carcinoma (NPC) cells, we evaluated the levels of miR‐143 and formin‐like protein 1 (FMNL1) in NPC tissues. The results of qRT‐PCR and Western blot analysis showed that the expression of miR‐143 was decreased, while FMNL1 was increased in NPC tissues. The expression of miR‐143 was significantly elevated in NPC cells compared with that of human nasopharyngeal epithelial cells. The results of MiRcode prediction, dual‐luciferase reporter, and Western blot analysis assays indicated that miR‐143 negatively regulated the expression of FMNL1 ( r 2 = 0.4365 P = 0.0001). Overexperssion of miR‐143 or FMNL1 knockdown inhibited cell proliferation, migration, and invasion in NPC cells ( P < 0.05). Ectopic expression of FMNL1 undermined the inhibition effect of miR‐143 on proliferation, migration, and invasion in NPC cells. The findings of this study revealed that miR‐143 functioned as a tumor suppressor and inhibited the NPC progression by targeting FMNL1.