PTPIP51 crosslinks the NFκB signaling and the MAPK pathway in SKBR3 cells

Author:

Dietel Eric1ORCID,Brobeil Alexander2,Tag Claudia1,Gattenloehner Stefan2,Wimmer Monika13

Affiliation:

1. Institute of Anatomy & Cell Biology, Justus-Liebig-University, Giessen 35392, Germany

2. Institute of Pathology, Justus-Liebig-University, Giessen 35392, Germany

3. Institute of Anatomy, Johannes-Kepler-University Linz, Linz 4040, Austria

Abstract

Aim: PTPIP51 interacts with NFκB signaling at the RelA and IκB level. NFκB signaling is linked to the initiation, progression and metastasis of breast cancer. Her2-amplified breast cancer cells frequently display activation of the NFκB signaling. We aimed to clarify the effects of NFκB inhibition on the NFκB- and MAPK-related interactome of PTPIP51 and cell viability in HaCat cells and SKBR3 cells. Results: IKK-16 selectively reduced cell viability in SKBR3 cells. PDTC induced a formation of the Raf1/14-3-3/PTPIP51 complex in SKBR3 cells, indicating a shift of PTPIP51 into MAPK signaling. Conclusion: IKK-16 selectively inhibits cell viability of SKBR3 cells. In addition, PTPIP51 might serve as the mediator between NFκB signaling and the MAPK pathway in SKBR3.

Publisher

Future Science Ltd

Subject

Biotechnology

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