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14 April 2019 : Clinical Research  

lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) Promotes Proliferation and Inhibits Apoptosis in Non-Small Cell Lung Cancer Cells by Regulating the miR-641/CDK6 Axis

Ya-Feng Fan1ABCE*, Zhong-Ping Yu1BCE, Xiao-Yan Cui1BE

DOI: 10.12659/MSM.913420

Med Sci Monit 2019; 25:2745-2755


BACKGROUND: The lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) gene has been reported as a potential oncogene in NSCLC. Nevertheless, the molecular mechanism of CRNDE in NSCLC progression remains largely unknown.

MATERIAL AND METHODS: qRT-PCR assay was performed to detect the expression levels of CRNDE, miR-641, and cyclin-dependent kinase 6 (CDK6) in NSCLC. Western blot assay was employed to assess CDK6 protein level in treated NSCLC cells. si-CRNDE#1, si-CRNDE#2, miR-641 mimics, miR-641 inhibitors, or Vector-CDK6 were transfected into NSCLC cells to change the expression levels of CRNDE, miR-641, or CDK6. Dual-luciferase reporter assay was performed to validate the direct interrelated miRNA of CRNDE and the potential target of miR-641. MTT and flow cytometry assays were performed to assess the capacities of cell proliferation and apoptosis, respectively.

RESULTS: CRNDE level was upregulated in NSCLC, and its knockdown suppressed NSCLC cells proliferation and enhanced apoptosis, whereas miR-641 antagonized the regulatory effect of CRNDE knockdown by directly binding to CRNDE. Moreover, CDK6 was a target of miR-641 and miR-641 exerted anti-proliferation and pro-apoptosis effects through CDK6.

CONCLUSIONS: CRNDE promoted proliferation and inhibited apoptosis of NSCLC cells at least in part by regulating the miR-641/CDK6 axis, suggesting that CRNDE is a potential therapeutic target for NSCLC treatment.

Keywords: Cyclin-Dependent Kinase 6, Disease Progression

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750