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

Eric Dietel; Alexander Brobeil; Claudia Tag; Stefan Gattenloehner; Monika Wimmer

doi:10.2144/fsoa-2019-0136

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

Future Sci OA. 2020 Mar 4;6(5):FSO463. doi: 10.2144/fsoa-2019-0136.

Authors

Eric Dietel¹, Alexander Brobeil², Claudia Tag¹, Stefan Gattenloehner², Monika Wimmer^{1

3}

Affiliations

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.

Keywords: Her2; IKK-16; NFκB; PDTC; PTPIP51; breast cancer; protein–protein interactions.