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. 2015 Mar 12;6(11):8914–8928. doi: 10.18632/oncotarget.3563

Figure 3. Re-expression of miR-203 in U251AR and U87AR cells sensitizes cells to anticancer drugs and reverses EMT while knockdown of miR-203 promotes resistance to anticancer drugs in U251 and U87 cells.

Figure 3

(A) qRT-PCR data validation of the downregulation of miR-203 in imatinib-resistant GBM cells compared with their parental cells, normalized to U6RNA, which was obtained from miRNA microarrays. (B, C) The sensitivities of U251AR and U87AR cells to imatinib, VP-16 and TMZ after transfected with miR-203 or miRNAs control. (D, E) Transfection with anti-miR-203 promotes resistance to imatinib, VP-16 and TMZ in U251 and U87 cells. (F) Morphology of U251AR and U87AR cells transfected with miRNA control or miR-203. Scale bar, 100 μm. (G) Western blotting show that re-expression of miR-203 modulates the expression of EMT markers. (H, I) U251AR and U87AR cells were transfected with miR-203 or anti-miR-203, and then collected for transwell invasion assay or wound healing assay. Shown were pictures of representative fields for each experiment. Scale bar, 200 μm. Data were expressed as mean±s.d. from three independent experiments. VP-16, etoposide; TMZ, temozolomide. *P < 0.05, **P < 0.01.