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LY6K miR-192-5p Compositions supportive for treating drug-resistanced breast cancer containing LY6K expression inhibitors or miR-192-5p inhibitors
LY6K miR-192-5p Compositions supportive for treating drug-resistanced breast cancer containing LY6K expression inhibitors or miR-192-5p inhibitors
The present invention relates to an anticancer drug-resistant breast cancer adjuvant comprising LY6K expression inhibitor or miR-192-5p inhibitor. The present invention discloses the mechanism of resistance to antihormonal drugs such as tamoxifen, which is a breast cancer therapeutic agent, 192-5 inhibition restores tamoxifen sensitivity by ERα re-expression, and provides a method of inhibiting the anticancer drug resistance and restoring the sensitivity to the anticancer drug. ERα is a clinically important therapeutic target in breast cancer. However, ERa loss causes tolerance to anti-estrogen drugs such as tamoxifen. The present inventors have found that LY6K associated with breast cancer cell proliferation and metastasis has an inverse correlation with ERa. ERα expression was down-regulated when LY6K was overexpressed in MCF-7 and T47D cells expressing ERα. In addition, we have shown that miR-192-5p targeting the 3'UTR of ESR1 in breast cancer is induced by LY6K gene expression. Luciferase assay revealed that miR-192-5p is regulated by LY6K and binds directly to the 3'UTR of ERa. In addition, miR-192-5p inhibition in LY6K-overexpressing cells restored tamoxifen sensitivity by re-expression of ERa. Thus, miR-192-5p, which is regulated by LY6K in breast cancer, inhibits ERα expression and endocrine resistance. Taken together, LY6K can play an important role in anticancer drug resistance through the suppression of ERα expression.
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