L-OHP resistant HT29 and HCT116 cells were exposed to escalating concentrations of L-OHP up to 30 μM. The effect of miR-200b-3p on L-OHP resistant CRC cells was then evaluated using the CCK8 assay. CRC cell apoptosis was detected using Annexin V-FITC/PI double staining. Bioinformatics algorithms and luciferase reporter assays were also performed to analyze whether TUBB3 was a direct target of miR-200b-3p.
miR-200b-3p declined in L-OHP resistant CRC tissues and cell lines, and the overexpression of miR-200b-3p elevated the L-OHP sensitivity in L-OHP resistant HT29 and HCT116 cells. In addition, we determined the potential mechanisms underlying miR-200b-3p-mediated reversal of L-OHP resistance via mediating its downstream target TUBB3, and the overexpression of miR-200b-3p could induce migration and growth inhibition and apoptosis in L-OHP resistant HT29 and HCT116 cells by silencing βIII-tubulin protein expression. However, the overexpression of TUBB3 reversed miR-200b-3p mimics-induced migration and growth inhibition and apoptosis in L-OHP resistant CRC cells.
miR-200b-3p improved L-OHP resistance and induced growth inhibition and cell apoptosis in L-OHP resistant CRC cells, and the underlying mechanism was mediated, at least partially, through the suppression of βIII-tubulin protein expression.
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