Cytochalasin D, a tropical fungal metabolite, inhibits CT26 tumor growth and angiogenesis

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Objective:To investigate whether cytochalasin D can induce antitumor activities in a tumor model.Methods: Murine CT26 colorectal carcinoma cells were culturedin vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibitingCT26 cell proliferation and inducing cell apoptosis by MTT and aTUNEL-based apoptosis assay. MurineCT26 tumor model was established to observe the tumor growth and survival time. Tumor tissues were used to detect the microvessel density by immunohistochemistry. In addition, alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results: Cytochalasin D inhibited CT26 tumor cell proliferation in time and dose dependent manner and induced significantCT26 cell apoptosis, which almost reached the level induced by the positive control nuclease. The optimum effective dose of cytochalasinD for in vivo therapy was about50 mg/kg. CytochalasinD in vivotreatment significantly inhibited tumor growth and prolonged the survival times inCT26 tumor-bearing mice. The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasinD could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibitsCT26 tumor growth potentially through inhibition of cell proliferation, induction of cell apoptosis and suppression of tumor angiogenesis.
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