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Ursolic acid potentiates paclitaxel induced antitumor effects on esophageal squamous cell carcinoma cell through the Akt signaling pathway

Development of chemoresistance, poor prognosis, and metastasis often renders the current treatments for esophageal cancer ineffective. The present research is designed to investigate ursolic acid (UA), a component of numerous medicinal plants, either alone or in combination with paclitaxel can inhibit the growth of esophageal squamous cell carcinoma (ESCC) through the Akt/FOXM1 signaling pathway. UA plus paclitaxel treatment inhibited the proliferation of TE‐12 and TE‐8 cells in a dose‐dependent manner when compared to treatment with UA or paclitaxel alone. In colony formation assay, UA potentiated the inhibition of colony formation by paclitaxel when compared to treatment with a single agent. Combination treatment induced apoptosis by increased levels of cleaved poly ADP‐ribose polymerase (PARP) and cleaved caspase‐9 protein and inhibited the invasion and metastasis of ESCC cells. In cell cycle analysis, UA plus paclitaxel induced the G1 cell cycle arrest when compared to treatment with UA or paclitaxel alone. In addition, UA potentiated paclitaxel‐induced inhibition of Akt function and increased phosphorylation form of Akt. These results suggest that UA effectively potentiates the efficacy of chemotherapeutic agents such as paclitaxel via inhibition of proliferation and increased apoptosis by inactivation of Akt in ESCC cells. Taken together, UA enhances the therapeutic efficacy of paclitaxel in esophageal cancer and is a potential clinical anticancer agent for the prevention and/or treatment of ESCC.