Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A
Authors Bian WX, Xue F, Wang LY, Xing XF
Received 7 September 2020
Accepted for publication 7 January 2021
Published 25 January 2021 Volume 2021:13 Pages 633—642
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Harikrishna Nakshatri
Wei-Xin Bian,1 Feng Xue,2 Li-Yan Wang,1 Xiao-Fang Xing1
1Department of Oncology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang Province 150001, People’s Republic of China; 2Department of Oncology, Affiliated Hospital of Guilin Medical College, Guilin, Guangxi Province 541001, People’s Republic of China
Correspondence: Wei-Xin Bian
Department of Oncology, Heilongjiang Provincial Hospital, Harbin, Heilongjiang Province 150001, People’s Republic of China
Aim: A series of research reveal that circular RNA (circRNA) plays a vital role in regulating the development of tumor cells. In this research, we would explore the role and mechanism of circCDYL in non-small cell lung cancer (NSCLC).
Methods: RT-PCR was performed to detect the expression of circCDYL in NSCLC tissues, plasma, and cell lines. The tumor cell proliferation ability was evaluated by clone formation assay, and cell cycle determination. Flow cytometry was used to detect apoptosis in NSCLC cell lines. Western blot and RT-PCR were used to assess the expression of proteins and genes. Luciferase assay was performed to confirm the relationship of circRNA-miRNA-mRNA.
Results: The decreased level of circCDYL was observed in NSCLC patients’ tissues and plasma, which was also downregulated in NSCLC cell lines. Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal.
Conclusion: Here, we revealed that circCDYL inhibited proliferation and induced apoptosis in NSCLC cell lines via regulating ERK1/2 signal, and the mechanism of this progression may target miR-185-5p/TNRC6A, which provided a theoretical basis for clinical therapy.
Keywords: non-small cell lung cancer, circular RNA, proliferation, apoptosis
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