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Background

Abnormal expression of NRF2 levels in some tumor tissues may enhance drug resistance through various mechanisms. Recent studies have demonstrated a link between dysregulated expression of miRNAs and breast carcinogenesis.

Methods

Quantitative RT-PCR analysis was used to examine the expression levels of miR-153 in breast cancer cell lines. The biological effects of miR-153 were assessed in CRC cell lines using clonogenic cell survival assay, mammosphere formation assay, cell migration assay, 8-OHdG estimation assay, and flow cytometry analysis. Quantitative RT-PCR and western blot analyses were employed to evaluate the expression of miR-153 targets. In this study, we investigated the role of vitamin C in the regulation of miR-153 (miR-153) and its target gene(s) in cell models of mammary carcinogenesis.

Results

In human breast cell lines treated with E2, the level of miR-153 was found to be increased. In contrast, vitamin C treatment was able to decrease the expression of miR-153. Bioinformatic prediction indicates nuclear factor erythroid 2-related factor 2 (NRF2) may be a target for miR-153. In E2-treated breast cancer cell lines, NRF2 protein level was found to be decreased. Overexpression of miR-153 significantly reduced NRF2 and the downstream genes. Furthermore, miR-153 was found to decrease apoptosis and increase colony formation in breast epithelial cells.

Conclusions

These data indicate that miR-153 acts as an oncogene in breast carcinogenesis by targeting NRF2."xsd:string
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