Home Neoplasma 2018 Neoplasma Vol.65, No.5, p.673-682, 2018

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Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

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Neoplasma Vol.65, No.5, p.673-682, 2018

Title: MiR-500a-3p inhibits cell proliferation and invasion by targeting lymphocyte antigen 6 complex locus K (LY6K) in human non-small cell lung cancer
Author: X.H. LIAO, Z. XIE, C.N. GUAN

Abstract: LY6K (lymphocyte antigen 6 complex locus K) is an anti-gene in non-small cell lung cancer (NSCLC) and miR-500a-3p promotes the progression of cancers. Evidence shows that increased miR-500a-3p caused LY6K suppression. Herein, we hypothesize that miR-500a-3p takes part in the progression of NSCLC through targeting LY6K. miR-500a-3p expression levels in NSCLC specimens and cell lines were detected by quantitative real-time PCR (qRT-PCR). The mRNA and protein expression levels of LY6K in NSCLC specimens and cell lines were examined by qRT-PCR, immunohistochemistry and western blotting. Dual-luciferase reporter assay assessed miR-500a-3p binding to the LY6K gene. The functions of miR-500a-3p and LY6K in proliferation/invasion and lung metastasis formation were assessed by CCK8, Transwell assay and subcutaneous tumor model in nude mice, respectively. Statistical analysis explored the clinical correlation between miR-500a-3p/LY6K expression and clinical-pathological features. While miR-500a-3p was substantially decreased in NSCLC tissues and cell lines. LY6K protein and mRNA level expressions were increased in NSCLC patients. Clinical analysis indicated that miR-500a-3p and LY6K were related to tumor differentiation, lymph node metastasis and TNM staging in NSCLC patients. MiR-500a-3p suppresses cell proliferation, invasion and metastasis formation in vivo by targeting the LY6K.miR-500a-3p acts as a tumor suppressor in NSCLC partly by down-regulating LY6K expression, and this suggests it is a potential therapeutic target for NSCLC intervention.

Keywords: LY6K; miR-500a-3p; non-small cell lung cancer; NSCLC, invasion; proliferation
Published online: 24-Sep-2018
Year: 2018, Volume: 65, Issue: 5 Page From: 673, Page To: 682

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