SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6
Authors Chen C, Zhang Z, Li J, Sun Y
Received 8 April 2018
Accepted for publication 11 July 2018
Published 20 September 2018 Volume 2018:11 Pages 6081—6090
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 4
Editor who approved publication: Dr Carlos E Vigil
Changhao Chen,1,* Zhiwei Zhang,2,* Jie Li,3 Yuejun Sun4
1Department of General Surgery, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210003, China; 2Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China; 3Department of Respiratory Medicine, Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu 214400, China; 4Department of Pathology, Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu 214400, China
*These authors contributed equally to this work
Background: Recently, various dynamically expressed lncRNAs are known to play critical roles in cancer progression. Small nucleolar RNA host genes (SNHG), a stable cytoplasmic lncRNA, which have been widely reported to act as an oncogene in non-small cell lung cancer (NSCLC). As an important member of SNHG, SNHG8 have been suggested to over-expressed in several cancer disease, while the biological function in NSCLC remains unclear.
Purpose: Here we investigated the biological function and underlying mechanism of SNHG8 in human NSCLC.
Patients and methods: The relationship between SNHG8 expression and clinicopathologic characteristic in NSCLC patients were observed from January 2014 to December 2014 in 120 NSCLC patients. The expression of SNHG8 were analyzed by qRT-PCR assay in cancer tissues and cells. Cell proliferation ability were detected in NSCLC cells by CCK-8 assay. Flow cytometric analysis were performed to detected the cell apoptosis and cell cycle. Luciferase assay and Western blot assay were performed on NSCLC cells to detected the underlying mechanism of SNHG8 in NSCLC. Moreover, Tumor xenografts in nude mice were performed to detected the in vivo function of SNHG8.
Results: SNHG8 was over-expressed in NSCLC tissues and cells. Patients with high SNHG8 expression have poorer overall survival (OS) and progression-free survival (PFS) than the patients with low SNHG8 expression. SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/CDK6, and induced cell apoptosis via activation of Caspase-3.
Conclusion: SNHG8 negatively regulated miR-542-3p in NSCLC progression by regulating downstream effectors including CCND1 and CDK6. SNHG8 showed great potential for the application in the treatment of NSCLC.
Keywords: SNHG8, non-small-cell lung cancer, cell proliferation, miR-542-3p, CCND1/CDK6, Caspase-3, cell proliferation, therapeutic target
Erratum for this paper has been published.
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