Vasoactive intestinal peptide (VIP) induces transactivation of EGFR and HER2 in human breast cancer cells

Ana Valdehita, Ana M. Bajo, Andrew V. Schally, Jozsef L. Varga, María J. Carmena, Juan C. Prieto

Research output: Contribution to journalArticlepeer-review

39 Scopus citations


We analyzed the cross-talk between receptors for vasoactive intestinal peptide (VIP) and the human epidermal growth factor family of tyrosine kinase receptors (HER) in oestrogen-dependent (T47D) and oestrogen-independent (MDA-MB-468) human breast cancer cells. VIP treatment slowly increased the expression levels of EGFR but it rapidly augmented phosphorylation of EGFR and HER2 in both cell lines. This pattern of HERs transactivation was blocked by the specific VIP antagonist JV-1-53, supporting the direct involvement of VIP receptors in formation of P-EGFR and P-HER2. VIP-induced transactivation was also abolished by H89 (protein kinase A inhibitor), PP2 (Src inhibitor) or TAPI-1 (inhibitor of matrix metalloproteases), following a differential pattern. These results shed a new light on the specific signalling pathways involved in EGFR/HER2 transactivation by VPAC receptors and suggest the potential usefulness of VIP receptor antagonists together with current antibodies against EGFR/HER2 and/or tyrosine kinase inhibitors for breast cancer therapy.

Original languageEnglish (US)
Pages (from-to)41-48
Number of pages8
JournalMolecular and Cellular Endocrinology
Issue number1
StatePublished - Apr 10 2009


  • Breast cancer
  • Drug treatment
  • EGFR
  • GHRH analogues
  • HER2
  • VIP receptors

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry


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