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

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

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

Author(s) -

Eric Dietel,

Alexander Brobeil,

Claudia Tag,

Stefan Gattenloehner,

Monika Wimmer

Publication year - 2020

Publication title -

future science oa

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.825

H-Index - 23

ISSN - 2056-5623

DOI - 10.2144/fsoa-2019-0136

Subject(s) - skbr3 , mapk/erk pathway , viability assay , hacat , nf κb , signal transduction , microbiology and biotechnology , cancer research , iκb kinase , cell signaling , chemistry , biology , cell , cancer cell , cancer , biochemistry , genetics , in vitro , human breast

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.

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