Abstract

Objectives Blood vessels provide convenient conditions for tumor cell proliferation and distant metastasis. Antiangiogenesis and proapoptosis of tumor cells have become critical means of clinically treating tumors. This study aimed to investigate the antiangiogenic and pro-apoptotic abilities of α-solanine. Methods This study used the CCK8 method to select appropriate drug concentrations. Next, the antitumor mechanism of α-solanine under hypoxia was investigated using wound healing, transwell, cellular immune, and Western blot assays. Finally, a reverse validation was performed by adding MHY1485, an mammalian targets of rapamycin ( mTOR) activator. Results α-Solanine significantly decreased B-cell lymphoma2-related protein , n-Ca, vascular endothelial growth factor , MMP2, and MMP9 expression in cells. In addition , Bax, p53, TIMP1, and E-Ca expressions were upregulated. However, this study found that adding MHY1485 significantly attenuated the effects of α-solanine. These results suggest that α-solanine may achieve these functions by regulating the PI3K/Akt/mTOR signaling pathway. Conclusion α-Solanine is highly resistant to angiogenesis and promotes apoptosis of M2 tumor-associated macrophages. These effects may depend on the PI3K/Akt/mTOR signaling pathway. The present study demonstrated that α-solanine has a strong anticancer effect under hypoxic conditions.

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