PTPIP51 crosslinks the NF?B signaling and the MAPK pathway in SKBR3 cells.
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ABSTRACT: Aim
PTPIP51 interacts with NF?B signaling at the RelA and I?B level. NF?B signaling is linked to the initiation, progression and metastasis of breast cancer. Her2-amplified breast cancer cells frequently display activation of the NF?B signaling. We aimed to clarify the effects of NF?B inhibition on the NF?B- 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 NF?B signaling and the MAPK pathway in SKBR3.
SUBMITTER: Dietel E
PROVIDER: S-EPMC7273389 | biostudies-literature | 2020 Mar
REPOSITORIES: biostudies-literature
Publications
PTPIP51 crosslinks the NFκB signaling and the MAPK pathway in SKBR3 cells.
Dietel Eric E Brobeil Alexander A Tag Claudia C Gattenloehner Stefan S Wimmer Monika M
Future science OA 20200304 5
<h4>Aim</h4>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.<h4>Results</h4>IKK-16 selectively reduced cell viability in SKBR3 cells. PDTC induced a for ...[more]
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