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LncRNA HCG11 Suppresses Cell Proliferation and Promotes Apoptosis via Sponging miR-224-3p in Non-Small-Cell Lung Cancer Cells

Authors Wang G, Liu L, Zhang J, Huang C, Chen Y, Bai W, Wang Y, Zhao K, Li S

Received 30 December 2019

Accepted for publication 19 May 2020

Published 3 July 2020 Volume 2020:13 Pages 6553—6563


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Carlos E Vigil

Guige Wang,1,2 Lei Liu,1,2 Jiaqi Zhang,1,2 Cheng Huang,1,2 Yeye Chen,1,2 Wenliang Bai,1,2 Yanqing Wang,1,2 Ke Zhao,1,2 Shanqing Li1,2

1Department of Thoracic Surgery, Peking Union Medical College Hospital, Beijing 100730, People’s Republic of China; 2Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, People’s Republic of China

Correspondence: Shanqing Li
Department of Thoracic Surgery, Peking Union Medical College Hospital, Shuaifuyuan No. 1 Dongcheng District, Beijing 100730, People’s Republic of China

Introduction: Studies have found that Lnc-HCG11 is an important regulator of cancer. However, the function of Lnc-HCG11 in NSCLC is not known. Therefore, this experimental design was based on Lnc-HCG11 to explore the pathogenesis of NSCLC.
Methods: RT-qPCR was used to detect the expression of Lnc-HCG11 and miR-224-3p in NSCLC. The effects of Lnc-HCG11 and miR-224-3p on proliferation and apoptosis of NSCLC cells were detected by CCK-8 assay, Edu assay and Annexin V-FITC/PI assay. Target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lnc-HCG11 and miR-224-3p. Western blotting was used to detect the protein expression of caspase-3. The tumor changes in mice were detected by in vivo.
Results: Lnc-HCG11 was significantly reduced in NSCLC. Lnc-HCG11 significantly inhibited cell proliferation of NSCLC cells and induced apoptosis. miR-224-3p was significantly elevated in the NSCLC cell line. Moreover, miR-224-3p significantly increased cell proliferation and inhibited apoptosis of NSCLC cells. Furthermore, Lnc-HCG11 was negatively correlated with miR-224-3p expression. Lnc-HCG11 over-expression was up-regulated the expression levels of c-caspase-3 and caspase-3. Finally, the results of in vivo animal models confirmed that Lnc-HCG11 inhibited tumor growth by modulating the miR-224-3p/c-caspase-3 axis.
Conclusion: Lnc-HCG11 could inhibit the progression of NSCLC by modulating the miR-224-3p/caspase-3 axis, and Lnc-HCG11 may be a potential therapeutic target for NSCLC.

Keywords: Lnc-HCG11, miR-224-3p, non-small-cell lung cancer, proliferation, apoptosis

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