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Tectorigenin suppresses the viability of gastric cancer cells in vivo and in vitro

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DOI: 10.15586/qas.v15i3.1357

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Apoptosis; cell cycle; gastric cancer; PI3K/Akt pathway; Tectorigenin (Tec)

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The study demonstrated that Tec effectively inhibited the viability and motility of gastric cancer cells, induced cell cycle arrest, and halted gastric cancer progression by suppressing the PI3K/Akt pathway.
Gastric cancer is currently the 4th most common malignant tumor with a poor prognosis in 2022. New and effective drugs are needed to combat this disease to treat advanced gastric cancer. Tectorigenin (Tec) has a series of pharmacological activities, such as anti-inflammatory and anticancer. However, the effect of Tec on the progression of gastric cancer is unclear. In this study, we investigated the role of Tec in regulating cell viability, cell cycle, and tumor growth of gastric cancer. To detect the role of Tec in the progression of gastric cancer in vitro and in mice, we performed several in vitro assays such as MTT, colony formation, wound closure, transwell, Immunoblot assays, and in vivo tumor growth assays. Our data confirmed that Tec restrained the viability of gastric cancer cells at concentrations of 100, 200, and 300 mu M. It also denied the motility of gastric cancer cells. Tec treatment also induced the cell cycle arrest of gastric cancer cells. Mechanically, Tec could suppress the activation of the PI3K/ Akt pathway and stop gastric cancer progression. We, therefore, thought Tec could serve as a drug for treating gastric cancer.

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