期刊
BIOMOLECULES
卷 12, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/biom12070891
关键词
Tetramethylpyrazine; epithelial-mesenchymal transition; MnSOD; TGF beta signaling
资金
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [NRF-2021R1I1A2060024, NRF-2022R1I1A1A01071593]
- Singapore Ministry of Education [MOE-T2EP30120-0016]
- National Research Foundation of Singapore (NUS R&G Postdoc Fellowship) [NUS-76]
This study demonstrates that 2,3,5,6-Tetramethylpyrazine (TMP) can suppress the EMT program in colon cancer cells by regulating MnSOD and related proteins, and inhibit the proliferation, migration, and invasion of tumor cells.
Epithelial-mesenchymal transition (EMT) is a crucial process in which the polarized epithelial cells acquire the properties of mesenchymal cells and gain invasive properties. We have previously demonstrated that manganese superoxide dismutase (MnSOD) can regulate the EMT phenotype by modulating the intracellular reactive oxygen species. In this report, we have demonstrated the EMT-suppressive effects of 2,3,5,6-Tetramethylpyrazine (TMP, an alkaloid isolated from Chuanxiong) in colon cancer cells. TMP suppressed the expression of MnSOD, fibronectin, vimentin, MMP-9, and N-cadherin with a parallel elevation of occludin and E-cadherin in unstimulated and TGF beta-stimulated cells. Functionally, TMP treatment reduced the proliferation, migration, and invasion of colon cancer cells. TMP treatment also modulated constitutive activated as well as TGF beta-stimulated PI3K/Akt/mTOR, Wnt/GSK3/beta-catenin, and MAPK signaling pathways. TMP also inhibited the EMT program in the colon cancer cells-transfected with pcDNA3-MnSOD through modulation of MnSOD, EMT-related proteins, and oncogenic pathways. Overall, these data indicated that TMP may inhibit the EMT program through MnSOD-mediated abrogation of multiple signaling events in colon cancer cells.
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