miR‐200b‐3p mitigates oxaliplatin resistance via targeting TUBB3 in colorectal cancer.

Background: Numerous abnormally expressed miRs have been reported involved in oxaliplatin (L‐OHP) resistance of colorectal cancer (CRC). The present study aimed to investigate whether miR‐200b‐3p could regulate L‐OHP resistance via targeting TUBB3 in CRC cells. Methods: 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 cell counting kit‐8 (CCK‐8) assay. CRC cell apoptosis was detected using Annexin V‐FITC/PI double staining. Bioinformatics algorithms and luciferase reporter assays were also performed to investigate whether TUBB3 was a direct target of miR‐200b‐3p. Results: 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 by 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 mimic‐induced migration, as well as growth inhibition and apoptosis, in L‐OHP resistant CRC cells. Conclusions: 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. [ABSTRACT FROM AUTHOR]