MicroRNA-21 inhibitor sensitizes human glioblastoma cells U251 (PTEN-mutant) and LN229 (PTEN-wild type) to taxol

摘要: Substantial data indicate that the oncogene microRNA 21 (miR-21) is significantly elevated in glioblastoma multiforme (GBM) and regulates multiple genes associated with cancer cell proliferation, apoptosis, invasiveness. Thus, miR-21 can theoretically become a target to enhance chemotherapeutic effect therapy. So far, of downregulating taxol has not been studied human GBM. Human U251 (PTEN-mutant) LN229 (PTEN wild-type) cells were treated inhibitor (in poly (amidoamine) (PAMAM) dendrimer), alone or combination. The 50% inhibitory concentration viability determined by MTT assay. mechanism between anticancer drug was analyzed using Zheng-Jun Jin method. Annexin V/PI staining performed, apoptosis cycle evaluated flow cytometry analysis. Expression investigated RT-PCR, western blotting performed evaluate malignancy related protein alteration. IC(50) values dramatically decreased combine taxol, greater extent than those alone. Furthermore, enhanced both cells, invasiveness obviously weakened. Interestingly, above suggested PTEN mutant wild-type GBM blockage increased chemosensitivity taxol. It worth noting additively interacted on U251cells synergistically cells. might interrupt activity EGFR pathways, independently status. Meanwhile, expression STAT3 p-STAT3 relatively low levels after treatment. strongly regulatory loop provide an insight into modulating EGFR/STAT3 signaling. Taken together, could chemo-sensitivity A combination be effective therapeutic strategy for controlling growth inhibiting phosphorylation.