Anti-LY6K (N-terminal) polyclonal antibody

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.

Purposes: To investigate the effect of proliferation, migration and invasion after knockdown LY6K in cervical cancer HeLa cells, and then clarify the potential mechanism. Methods: The expression of LY6K in cervical cancer tissues was determined by S-P immunohistochemistry. The proliferation, migration and invasion ability were detected after silencing LY6K in cervical cancer HeLa cell lines. The expression of VEGFA, miR-15a and miR-24 was detected after knockdown LY6K in cervical cancer HeLa cells. The expression of LY6K and VEGFA was detected when transfected miR-15a mimics and miR-24 mimics. Then we determined the tumorigenicity of cervical cancer HeLa cells after knockdown LY6K. Results: The expression of LY6K was higher in cervical cancer tissues than normal cervical tissues (P<0.05). The proliferation, migration and invasion ability were decreased after silencing LY6K in cervical cancer HeLa cells (P<0.05). The expression of VEGFA was decreased after knockdown LY6K; however, the expression of miR-15a and miR-24 was increased after knockdown LY6K (P<0.05). The expression of LY6K was decreased after knockdown VEGFA; however, the expression of miR-15a and miR-24 was increased after knockdown VEGFA (P<0.05). The expression of LY6K and VEGFA was inhibited when transfected miR-15a and miR-24; however, the expression of LY6K and VEGFA was increased when transfected miR-15a and miR-24 inhibitors (P<0.05). Silencing LY6K prevented cervical cancer growth in vivo. Conclusion: Silencing LY6K can inhibited proliferation, migration and invasion ability in cervical HeLa cells by regulation VEGFA.