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Molecular Carcinogenesis

Molecular Carcinogenesis

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γ-Tocotrienol enhances autophagy of gastric cancer cells by the regulation of GSK3β/β-Catenin pathway

Published:1 October 2024 DOI: 10.1002/mc.23790 PMID: 38980215
Hao Zhu,?Fa-Lin Wang,?Shuang Zhang,?Li Xue,?Guang-Qiang Gao,?Hong-Wei Dong,?Qi Wang,?Wen-Guang Sun,?Jia-Ren Liu

Abstract

γ-Tocotrienol (γ-T3) is a major subtype of vitamin E, mainly extracted from palm trees, barley, walnuts, and other plants. γ-T3 has effects on anti-inflammation, anti-oxidation, and potential chemoprevention against malignancies. It is still uncompleted to understand the effect of γ-T3 on the inhibitory mechanism of cancer. This study aimed to investigate whether γ-T3 enhanced autophagy in gastric cancer and the underlying molecular mechanism. The results showed that γ-T3 (0-90?μmol/L) inhibited the proliferation of gastric cancer MKN45 cells and AGS cells, and arrested the cell cycle at the G0/G1 phase in a dose-dependent manner. Autophagy was increased in MKN45 cells treated with γ-T3 (0-45?μmol/L), especially at a dose of 30?μmol/L for 24?h. These effects were reversed by 3-methyladenine?pretreatment. Furthermore, γ-T3 (30?μmol/L) also significantly downregulated the expression of pGSK-3β (ser9) and β-catenin protein in MKN45 cells, and γ-T3 (20?mg/kg b.w.) effectively decreased the growth of MKN45 cell xenografts in BABL/c mice. GSK-3β inhibitor-CHIR-99021 reversed the negative regulation of GSK-3β/β-Catenin signaling and autophagy. Our findings indicated that γ-T3 enhances autophagy in gastric cancer cells mediated by GSK-3β/β-Catenin signaling, which provides new insights into the role of γ-T3 enhancing autophagy in gastric cancer.

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3-METHYLADENINE 5142-23-4 C6H7N5 393 suppliers $12.00-$4500.00
3-METHYLADENINE 5142-23-4 C6H7N5 393 suppliers $12.00-$4500.00
3-METHYLADENINE 5142-23-4 C6H7N5 393 suppliers $12.00-$4500.00
3-METHYLADENINE 5142-23-4 C6H7N5 393 suppliers $12.00-$4500.00
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3H-?Purin-?6-?amine, 3-?methyl- 5142-23-4 C6H7N5 - Inquiry

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