Abstract

BackgroundGlioblastoma multiforme (GBM) is one of the most aggressive brain tumors among human beings. In this study, we explored the functions of human microRNA-1270 (hsa-miR-1270) on GBM cancer cell proliferation, migration, and tumorigenesis.Materials and methodsIn GBM cell lines and clinical tissues, hsa-miR-1270 expression was probed by quantitative real-time PCR (qRT-PCR). In LN-18 and A172 cells, hsa-miR-1270 was upregulated by lentiviral transduction. The effects of hsa-miR-1270 upregulation on GBM in vitro and in vivo functions were probed by proliferation, migration, and xenograft assays, respectively. The correlation between hsa-miR-1270 and Wilms’ tumor gene (WT1) was probed by dual-luciferase activity assay, qRT-PCR, and Western blot. WT1 was then secondarily over-expressed in hsa-miR-1270-upregulated LN-18 and A172 cells, to explore its mechanisms in GBM’s association with hsa-miR-1270.ResultsHsa-miR-1270 was significantly downregulated in both GBM cell lines and clinical tumors. Upregulating hsa-miR-1270 considerably suppressed GBM cell proliferation and migration in vitro and xenograft in vivo. WT1 was inversely correlated with hsa-miR-1270 in GBM. WT1 overexpression in hsa-miR-1270-upregulated GBM cells reversed the anticancer functions of hsa-miR-1270 on cancer proliferation and migration.ConclusionHsa-miR-1270 upregulation may have suppressing effects on GBM cancer cells, likely by functionally acting through WT1.

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.