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Significance CRC patients withKRAS mutations are confronted with limited targeted therapeutic options. In this study, we have shown that the median survival time forKRAS -mutation mCRC patients with diabetes on metformin is 37.8 mo longer than those treated with other hypoglycemic drugs in combination with standard systemic therapy. Metformin is preferentially accumulated inKRAS -mutation CRC cells in both primary cell cultures and patient-derived xenografts. The promising therapeutic activity of metformin has a negative correlation with MATE1 expression, which is proven to eliminate metformin from CRC cells. These findings indicate thatKRAS -mutation mCRC patients could benefit from metformin treatment, and somaticKRAS status or MATE1 expression should be recommended to predict the therapeutic response of metformin in CRC.

Metformin selectively inhibits metastatic colorectal cancer with the KRAS mutation by intracellular accumulation through silencing MATE1