Please use this identifier to cite or link to this item: https://doi.org/10.3390/biom12070891
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dc.title2,3,5,6-Tetramethylpyrazine Targets Epithelial-Mesenchymal Transition by Abrogating Manganese Superoxide Dismutase Expression and TGF beta-Driven Signaling Cascades in Colon Cancer Cells
dc.contributor.authorJung, Young Yun
dc.contributor.authorMohan, Chakrabhavi Dhananjaya
dc.contributor.authorEng, Huiyan
dc.contributor.authorNarula, Acharan S
dc.contributor.authorNamjoshi, Ojas A
dc.contributor.authorBlough, Bruce E
dc.contributor.authorRangappa, Kanchugarakoppal S
dc.contributor.authorSethi, Gautam
dc.contributor.authorKumar, Alan Prem
dc.contributor.authorAhn, Kwang Seok
dc.date.accessioned2023-02-14T01:09:17Z
dc.date.available2023-02-14T01:09:17Z
dc.date.issued2022-07-01
dc.identifier.citationJung, 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
dc.identifier.issn2218-273X
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/237181
dc.description.abstractEpithelial-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.
dc.language.isoen
dc.publisherMDPI
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectTetramethylpyrazine
dc.subjectepithelial-mesenchymal transition
dc.subjectMnSOD
dc.subjectTGF beta signaling
dc.subjectGROWTH-FACTOR-BETA
dc.subjectOXIDATIVE STRESS
dc.subjectBREAST-CANCER
dc.subjectWNT/BETA-CATENIN
dc.subjectSTAT3 ACTIVATION
dc.subjectTUMOR-GROWTH
dc.subjectIN-VITRO
dc.subjectMETASTASIS
dc.subjectSUPPRESSION
dc.subjectINHIBITION
dc.typeArticle
dc.date.updated2023-02-13T06:28:50Z
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.3390/biom12070891
dc.description.sourcetitleBIOMOLECULES
dc.description.volume12
dc.description.issue7
dc.published.statePublished
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