IKKα controls canonical TGFβ–SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in Panc1 cells
作者： M. Brandl , B. Seidler , F. Haller , J. Adamski , R. M. Schmid
DOI: 10.1242/JCS.071100
关键词:
摘要: The epithelial to mesenchymal transition (EMT) is a crucial step in tumor progression, and the TGFβ-SMAD signaling pathway an inductor of EMT many types. One hallmark downregulation adherens junction protein E-cadherin, process mediated by transcription factors such as zinc fingers SNAIL SLUG. Here, we report that catalytic IκB kinase (IKK) subunit IKKα necessary for silencing E-cadherin Panc1 cell model TGFβ-SMAD-mediated EMT, independently NFκB. regulates canonical interacting with SMAD3 controlling SMAD complex formation on DNA. Furthermore, demonstrate TGFβ-IKKα-SMAD induces genes encoding In addition, also modulates human MDA-MB231 breast cancer cells, arguing more general impact control signaling. Taken together, these findings indicate contributes tumor-promoting function particular cancers.
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