MiR-652-3p is upregulated in non-small cell lung cancer and promotes proliferation and metastasis by directly targeting Lgl1
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Wenhui Yang1, Chengcheng Zhou1, Mei Luo1, Xuejiao Shi1, Yuan Li1, Zengmiao Sun1, Fang Zhou1, Zhaoli Chen1, Jie He1
1Department of Thoracic Surgery, Cancer Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100021, China
Zhaoli Chen, e-mail: firstname.lastname@example.org
Jie He, e-mail: email@example.com
Keywords: miR-652-3p, Lgl1, NSCLC, proliferation, metastasis
Received: August 11, 2015 Accepted: February 09, 2016 Published: February 25, 2016
Our previous study found that miR-652-3p is markedly upregulated in the serum of patients with NSCLC and suggesting that miR-652-3p is a potential biomarker for the early diagnosis of NSCLC. In this study, we detected the expression of miR-652-3p in NSCLC tumor tissues and cell lines and investigated the effect of miR-652-3p on the proliferation and metastasis of NSCLC cells. Our results showed that the expression of miR-652-3p was significantly upregulated in tumor tissues of 50 patients with NSCLC, and it was significantly higher in patients with positive lymph node metastasis, advanced TNM stage and poor prognosis. Using functional analyses by overexpressing or suppressing miR-652-3p in NSCLC cells, we demonstrated that miR-652-3p promoted cell proliferation, migration, invasion and inhibited cell apoptosis. Moreover, the lethal(2) giant larvae 1 (Lgl1) was identified as a direct and functional target of miR-652-3p. Overexpression or knockdown of miR-652-3p led to decreased or increased expression of Lgl1 protein, and the binding site mutation of LLGL1 3’UTR abrogated the responsiveness of the luciferase reporters to miR-652-3p. Overexpression of Lgl1 partially attenuated the function of miR-652-3p. Collectively, these results revealed that miR-652-3p execute a tumor-promoter function in NSCLC through direct binding and regulating the expression of Lgl1.
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