Abstract

MicroRNAs (miRNAs) have been reported to be involved in tumorigenesis. The aim of this study was to investigate the functional role and prognostic value of miR-652 in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression levels of miR-652 in human GC tissue samples and GC cell lines. The Kaplan-Meier survival curves and Cox regression analysis were performed to measure the prognostic value of miR-652 in GC. The tumor cell proliferation capacity was estimated by MTT assay, and cell migration and invasion were assessed by Transwell assays. The luciferase reporter assay was performed to confirm the target gene of miR-652. MiR-652 was significantly elevated in GC tissues and cell lines (all P< 0.001). And the expression level of miR-652 was significantly associated with TNM stage and lymph node metastasis (all P< 0.05). GC patients with high expression of miR-652 had a shorter overall survival rate than those with low miR-652 expression (log-rank P< 0.001). The miR-652 and TNM stage were proven to be independent prognostic predictors for the GC patients. Overexpressing miR-652 could enhance cell proliferation, migration and invasion (all P< 0.01). RORA was proved to be the target gene of miR-652. MiR-652 functions as an oncogene in GC and promotes tumor progression via targeting RORA. MiR-652 might be a novel predictive marker for the poor prognosis of GC patients.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.