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Phosphoproteome of signaling by ErbB2 in ovarian cancer cells

C Sidhanth1, S Bindhya1, S Krishnapriya1

  • 1Laboratory for Cancer Biology, Departments of Medical Oncology and Clinical Research, Cancer Institute (WIA), Chennai, India.

Biochimica Et Biophysica Acta. Proteins and Proteomics
|February 14, 2022
PubMed

Insights

Researchers identified novel ErbB2-specific phosphoproteins in ovarian cancer cells using mass spectrometry. These findings advance understanding of ErbB2 signaling pathways and potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Receptor tyrosine kinase ErbB2 amplification is common in breast and ovarian cancers.
  • While linear ErbB2 signaling pathways are known, spatial signaling aspects require further investigation.

Purpose of the Study:

  • To identify phosphoproteins specifically associated with ErbB2 signaling in ovarian cancer cells.
  • To investigate the effects of ErbB2 inhibitors Lapatinib and CP724714 on these phosphoproteins.

Main Methods:

  • Mass spectrometry was employed to identify phosphoproteins in SKOV-3 ovarian cancer cells.
  • Cells were treated with ErbB2 inhibitors Lapatinib and CP724714, and epidermal growth factor (EGF).
  • The phosphorylation status and activity of specific proteins (PKM2, Aldose Reductase, MARCKS) were evaluated.

Main Results:

  • Several ErbB2-specific phosphoproteins were identified, including MARCKS, which showed ErbB2 kinase-dependent phosphorylation inhibited by Lapatinib and CP724714.
  • Aldose reductase activity increased with EGF stimulation and was inhibited by Lapatinib and CP724714, but not Gefitinib.
  • PKM2 phosphorylation by EGF was not affected by Lapatinib or CP724714.

Conclusions:

  • Novel phosphoproteins specific to ErbB2 signaling in ovarian cancer have been identified.
  • These findings provide a foundation for future research into ErbB2-mediated spatial signaling and therapeutic strategies.
Keywords:
ErbB2Ovarian cancerPhosphoproteomeSignaling

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