MiR-500a-3p inhibits cell proliferation and invasion by targeting lymphocyte antigen 6 complex locus K (LY6K) in human non-small cell lung cancer

被引:17
作者
Liao, X. H. [1 ]
Xie, Z. [1 ]
Guan, C. N. [2 ]
机构
[1] Guangdong Med Univ, Affiliated Hosp 1, Dept Oncol, Zhanjiang, Peoples R China
[2] Guangdong Med Univ, Canc Ctr, Dongguan, Peoples R China
关键词
LY6K; miR-500a-3p; non-small cell lung cancer; NSCLC; invasion; proliferation; EXPRESSION; APOPTOSIS; MICRORNAS; GENE;
D O I
10.4149/neo_2018_170516N355
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:673 / 682
页数:10
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