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

Wenchong Song; Weiwei Lv; Ning Bi; Guanglin Wang

doi:10.15586/qas.v15i3.1357

Wenchong Song

Second ward of Gastroenterology, Huanggang Central Hospital affiliated to Changjiang University, Huanggang, China.

Weiwei Lv

Department of Pharmacy, Huanggang Central Hospital affiliated to Changjiang University, Huanggang, China.

Ning Bi

Second ward of Gastroenterology, Huanggang Central Hospital affiliated to Changjiang University, Huanggang, China.

Guanglin Wang

Second ward of Gastroenterology, Huanggang Central Hospital affiliated to Changjiang University, Huanggang, China.

Keywords

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

Abstract

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 μM. 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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