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03 February 2020 : Laboratory Research

MiR-323-3p Targeting Transmembrane Protein with EGF-Like and 2 Follistatin Domain (TMEFF2) Inhibits Human Lung Cancer A549 Cell Apoptosis by Regulation of AKT and ERK Signaling Pathways

Ji-min Fan1ACE, Zheng-rong Zheng2ACEF, Yi-Ming Zeng1BCF, Xiao-yang Chen1BCF*

DOI: 10.12659/MSM.919454

Med Sci Monit 2020; 26:e919454

Abstract

BACKGROUND: Non-small-cell lung cancer (NSCLC) is predominant and has low 5-year relative survival rate. Therefore, the mechanisms of NSCLC tumorigenesis must be comprehensively elucidated. MicroRNA-323-3p (miR-323-3p) has been widely explored and found to exert functions in tumorigenesis of several cancer types. However, the expression pattern and biological function of miR-323-3p and the molecular mechanism underlying NSCLC development and progression remain unclear.

MATERIAL AND METHODS: Quantitative reverse-transcription polymerase chain reaction was used to detect the expression of miR-323-3p and TMEFF2 in NSCLC cell lines (A549, NCI-H3255, and H1299) and normal cell line (BEAS-2B). Methylthiazolyl tetrazolium, colony formation, and flow cytometry assays were performed to evaluate the effects of miR-323-3p and TMEFF2 on cell proliferation. Transwell assay was conducted to determine the effects of TMEFF2 on cell migration and invasion. Dual-luciferase reporter assay was used to verify whether TMEFF2 is a target of miR-323-3p. Western blot analysis was performed to analyze protein expression.

RESULTS: The expression of miR-323-3p increased in the 3 NSCLC cell lines (A549, NCI-H3255, and H1299). miR-323-3p regulated cellular progression by directly suppressing TMEFF2 expression and indirectly prohibited the activation of AKT and ERK pathways in NSCLC.

CONCLUSIONS: Overall, miR-323-3p was considered a lung cancer oncogene and could be a valuable target for NSCLC therapy.

Keywords: Cellular Microenvironment

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