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Involvement of PI3K/AKT and beta‐catenin signaling in anti‐cancer activity of 7‐O‐succinyl macrolactin A (842.4)

Colorectal cancer is the 4th most common cancer and the second most common cause of cancer‐related death in the world. One of the most commonly involved pathways in cancer cell survival, growth and proliferation is the PI3K/AKT/mTOR pathway. In addition, Wnt/beta‐catenin signaling pathway has been implicated in colorectal tumorigenesis by upregulating genes related to cell proliferation such as c‐Myc and cyclin D1. In the present study, we investigated anti‐cancer activities of macrolactin A (MA) and its derivative, 7‐O‐succinyl macrolactin A (SMA) was mediated through PI3K/AKT/mTOR and beta‐catenin signaling. In the growth‐arrested HT‐29 cells by SMA, which was revealed by proliferation and colony formation assays, phosphorylation of PI3K/AKT/mTOR was suppressed. In addition, SMA inhibited Wnt‐induced beta‐catenin nuclear translocation and TCF/LEF transcriptional activity. Western blot analyses showed that SMA inhibited serum‐induced c‐Myc, cyclin D1, and survivin expressions in colon cancer cells. Taken together, the results suggest that anti‐cancer activity of SMA was mediated through both PI3K/AKT signaling and beta‐catenin pathway in colon cancer cells.