LncRNA HCP5 Stimulates the Proliferation of Non-Small Cell Lung Cancer Cells by Up-Regulating Survivin Through the Down-Regulation of miR-320
Authors Li C, Lei Z, Peng B, Zhu J, Chen L
Received 6 July 2019
Accepted for publication 10 October 2019
Published 14 February 2020 Volume 2020:12 Pages 1129—1134
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Professor Lu-Zhe Sun
Chao Li,1 Zhang Lei,2 Bin Peng,1 Jiang Zhu,1 Li Chen3
1Oncology Department, Second People’s Hospital of Jingmen, Jingmen City, Hubei Province 448000, People’s Republic of China; 2Department of Oncology, The Central Hospital of Wuhan Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan City, Hubei Province 430061, People’s Republic of China; 3Department of Traditional Chinese Medicine, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Art and Science, Xiangyang City, Hubei Province 441021, People’s Republic of China
Correspondence: Li Chen
Department of Traditional Chinese Medicine, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Art and Science, Jingzhou Street 136#, Xiangyang City, Hubei Province 441021, People’s Republic of China
Tel +86 0710-3522791
Introduction: We explored the roles of lncRNA HCP5 in non-small cell lung cancer (NSCLC).
Methods: Levels of HCP5 were measured by performing qPCR and data were compared between non-tumor and NSCLC tissue samples by performing a paired t-test. Expression levels of miR-320 and survivin mRNA in NSCLC tissues were also measured by performing qPCR. The effects of HCP5, miR-320 and survivin overexpression on the proliferation of H23 cells were analyzed by cell proliferation assay.
Results: We found that HCP5 was up-regulated in NSCLC and predicted the poor survival of NSCLC patients. HCP5 was negatively correlated with miR-320 but positively correlated with survivin in NSCLC tissues. In NSCLC cells, HCP5 overexpression led to the up-regulated survivin and down-regulated miR-320. Moreover, miR-320 overexpression failed to affect HCP5 but down-regulated survivin. Cell proliferation assay showed that HCP5 and survivin overexpression led to increased, while miR-320 overexpression led to decreased cell proliferation rate. In addition, miR-320 overexpression reduced the effects of HCP5 overexpression.
Conclusion: Therefore, HCP5 may stimulate the proliferation of NSCLC cells by up-regulating survivin through the down-regulation of miR-320.
Keywords: HCP5, non-small cell lung cancer, miR-320, survivin
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