PuSH - Publikationsserver des Helmholtz Zentrums München: IKKα controls canonical TGFß-SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in panc1 cells.

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Brandl, M.* ; Seidler, B.* ; Haller, F. ; Adamski, J. ; Schmid, R.M.* ; Saur, D.* ; Schneider, G.*

IKKα controls canonical TGFß-SMAD signaling to regulate genes expressing SNAIL and SLUG during EMT in panc1 cells.

J. Cell Sci. 123, 4231-4239 (2010)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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

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