Rabbit Anti-Human NCK1 Polyclonal antibody

Long non-coding RNA NCK1-antisense 1 (AS1) has recently been demonstrated to promote cell proliferation and induce cell cycle progression through the crosstalk NCK1-AS1/microRNA (miR)-6857/cyclin dependent kinase 1 pathway in cervical cancer. However, the regulatory mechanism of NCK1-AS1 in cervical cancer growth and metastasis remains largely unclear. In the present study, it was identified that NCK1-AS1 was significantly upregulated in cervical cancer tissues compared with the levels in adjacent non-tumour tissues. High expression levels of NCK1-AS1 were associated with tumour progression and poor prognosis in patients with cervical cancer. Silencing of NCK1-AS1 expression significantly decreased the levels of proliferation and migration of cervical cancer cells, and decreased the protein expression levels of matrix metalloproteinase (MMP)-2 and MMP-9. The results of the luciferase reporter gene assay indicated that there was an miR-134 binding site within the NCK1-AS1 gene in cervical cancer cells. miR-134 was significantly downregulated in cervical cancer tissues compared with the miR-134 levels in adjacent non-tumour tissues, and the expression level of miR-134 was inversely correlated with the NCK1-AS1 expression levels in cervical cancer tissues. Knockdown of miR-134 attenuated the inhibitory effects of NCK1-AS1 downregulation on the proliferation and migration of cervical cancer cells. Therefore, the data from the present study suggested that NCK1-AS1 serves a promotive role in cervical cancer cell proliferation and migration by functioning as a molecular sponge for miR-134. NCK1-AS1 may become a novel therapeutic target for cervical cancer.

Objective: This study aimed at probing into the effect of lncRNA NCK1-AS1 on proliferation, migration and in-vasion of non-small cell lung cancer (NSCLC) cells and its regulatory function on miR-512-5p/p21 molecular axis. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess the expressions of NCK1-AS1 and miR-512-5p in NSCLC tissues and cell lines. The alterations of cell proliferation, migration, in-vasion and cell cycle were examined by cell counting kit-8 (CCK-8) assay, BrdU experiment, Transwell experiment and flow cytometry, respectively. The dual-luciferase reporter assay and RNA immunoprecipitation experiment were performed to validate the binding relationships between miR-512-5p and NCK1-AS1, and miR512-5p the 3'UTR of p21 mRNA. Western blot was used to determine the effects of NCK1-AS1 and miR-512-5p on p21 protein expression. Results: NCK1-AS1 expression was up-regulated in NSCLC tissues and cells, and its high expression was correlated with shorter overall survival time and faster progression of patients. Overexpression of NCK1-AS1 promoted NSCLC cell proliferation, migration and invasion, and accelerated the cell cycle, whereas NCK1-AS1 siRNA inhibited these malignant biological behaviors, and arrested cell cycle. NCK1-AS1 could bind to miR-512-5p, p21 was verified as a target gene of miR-512-5p, and NCK1-AS1 could up-regulate the expression of p21 in NSCLC cells via repressing miR-512-5p expression. Conclusion: NCK1-AS1 promotes NSCLC progression by regulating miR-512-5p/p21 molecular axis.