Please use this identifier to cite or link to this item: https://doi.org/10.3390/biom12070891
Title: 2,3,5,6-Tetramethylpyrazine Targets Epithelial-Mesenchymal Transition by Abrogating Manganese Superoxide Dismutase Expression and TGF beta-Driven Signaling Cascades in Colon Cancer Cells
Authors: Jung, Young Yun
Mohan, Chakrabhavi Dhananjaya
Eng, Huiyan
Narula, Acharan S
Namjoshi, Ojas A
Blough, Bruce E
Rangappa, Kanchugarakoppal S
Sethi, Gautam 
Kumar, Alan Prem 
Ahn, Kwang Seok
Keywords: Science & Technology
Life Sciences & Biomedicine
Biochemistry & Molecular Biology
Tetramethylpyrazine
epithelial-mesenchymal transition
MnSOD
TGF beta signaling
GROWTH-FACTOR-BETA
OXIDATIVE STRESS
BREAST-CANCER
WNT/BETA-CATENIN
STAT3 ACTIVATION
TUMOR-GROWTH
IN-VITRO
METASTASIS
SUPPRESSION
INHIBITION
Issue Date: 1-Jul-2022
Publisher: MDPI
Citation: Jung, Young Yun, Mohan, Chakrabhavi Dhananjaya, Eng, Huiyan, Narula, Acharan S, Namjoshi, Ojas A, Blough, Bruce E, Rangappa, Kanchugarakoppal S, Sethi, Gautam, Kumar, Alan Prem, Ahn, Kwang Seok (2022-07-01). 2,3,5,6-Tetramethylpyrazine Targets Epithelial-Mesenchymal Transition by Abrogating Manganese Superoxide Dismutase Expression and TGF beta-Driven Signaling Cascades in Colon Cancer Cells. BIOMOLECULES 12 (7). ScholarBank@NUS Repository. https://doi.org/10.3390/biom12070891
Abstract: 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 TGFβ-stimulated cells. Functionally, TMP treatment reduced the proliferation, migration, and invasion of colon cancer cells. TMP treatment also modulated constitutive activated as well as TGFβ-stimulated PI3K/Akt/mTOR, Wnt/GSK3/β-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.
Source Title: BIOMOLECULES
URI: https://scholarbank.nus.edu.sg/handle/10635/237181
ISSN: 2218-273X
DOI: 10.3390/biom12070891
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