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

Eric Dietel1, Alexander Brobeil2, Claudia Tag1

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

Future Science OA
|June 11, 2020
PubMed
Abstract

Insights

NFκB inhibition selectively reduced SKBR3 breast cancer cell viability. PTPIP51 protein may mediate between NFκB and MAPK pathways, impacting cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Nuclear factor kappa B (NFκB) signaling is implicated in breast cancer initiation, progression, and metastasis.
  • Her2-amplified breast cancer often exhibits activated NFκB signaling.
  • PTPIP51 protein is known to interact with NFκB signaling components.

Purpose of the Study:

  • To investigate the effects of NFκB inhibition on the PTPIP51 interactome within NFκB and MAPK signaling pathways.
  • To assess the impact of NFκB inhibition on cell viability in HaCat and SKBR3 cells.

Main Methods:

  • Utilized IKK-16 and PDTC as NFκB inhibitors.
  • Analyzed PTPIP51 protein interactions within NFκB and MAPK pathways.
  • Assessed cell viability in HaCat and SKBR3 cell lines.

Main Results:

  • IKK-16 selectively reduced cell viability in SKBR3 cells.
  • PDTC treatment led to the formation of a Raf1/14-3-3/PTPIP51 complex in SKBR3 cells.
  • This complex formation suggests a translocation of PTPIP51 into the MAPK signaling pathway.

Conclusions:

  • IKK-16 demonstrates selective inhibition of cell viability in SKBR3 cells.
  • PTPIP51 may act as a crucial mediator connecting NFκB signaling to the MAPK pathway in SKBR3 cells.
  • These findings highlight potential therapeutic targets for Her2-amplified breast cancer.
Keywords:
Her2IKK-16NFκBPDTCPTPIP51breast cancerprotein–protein interactions

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