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

被引：49

作者：

Valdehita, Ana ^{[1
]}

Bajo, Ana M. ^{[1
]}

Schally, Andrew V. ^{[2
,3
,4
,5
]}

Varga, Jozsef L. ^{[2
,3
,4
,5
]}

Carmena, Maria J. ^{[1
]}

Prieto, Juan C. ^{[1
]}

机构：

[1] Univ Alcala de Henares, Mol Neuroendocrinol Unit, Dept Biochem & Mol Biol, Alcala De Henares 28871, Spain

[2] Univ Miami, Miller Sch Med, Vet Adm Med Ctr, Miami, FL 33125 USA

[3] Univ Miami, Miller Sch Med, Dept Pathol, Div Hematol & Oncol, Miami, FL 33125 USA

[4] Univ Miami, Miller Sch Med, Dept Med, Div Hematol & Oncol, Miami, FL 33125 USA

[5] S Florida Vet Affairs Fdn Res & Educ, Miami, FL 33125 USA

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 2009年 / 302卷 / 01期

关键词：

Breast cancer; VIP receptors; EGFR; HER2; GHRH analogues; Drug treatment; GROWTH-FACTOR RECEPTOR; HORMONE-RELEASING-HORMONE; PROTEIN-COUPLED RECEPTORS; TYROSINE KINASE; PROSTATE-CANCER; FAMILY; INHIBIT; ZD1839; ANTAGONISTS; EXPRESSION;

D O I：

10.1016/j.mce.2008.11.024

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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-I (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. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

引用

页码：41 / 48

页数：8

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