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Growth stimulatory angiotensin II type-1 receptor is upregulated in breast hyperplasia and in situ carcinoma but not in invasive carcinoma

Boel De Paepe (UGent) , Valerie Verstraeten, Christian De Potter, Luc Vakaet (UGent) and Gillian Bullock
(2001) HISTOCHEMISTRY AND CELL BIOLOGY. 116(3). p.247-254
Author
Organization
Abstract
Two different receptors which bind angiotensin II specifically have been identified in humans and were designated angiotensin II type-1 receptor (AT(1)) and angiotensin II type-2 receptor (AT(2)). They only have 34% sequence homology and act through different signalling pathways. AT(1) stimulation has been implicated in hypertrophy and hyperplasia in various tissues. In order to study the involvement of AT(1) in tissues from controls (n=10) and patients with hyperplasia (n=33), ductal carcinoma in situ (DCIS) (n=23) and invasive carcinoma of the breast (n=25), we tested biopsies and breast-derived cell lines using immunocytochemistry, in situ hybridisation and cell proliferation techniques. The results show specific overexpression of AT(1) receptor on the cytoplasmic membrane of cells of hyperplastic lesions with and without atypia and on DCIS of the breast. Evidence for growth stimulation is provided by in vitro experiments showing growth induction by angiotensin II of T47D cells which express the AT(1) but not the AT(2) receptor. The expression of AT(1) on the cell membrane disappears in invasive breast cancer cells suggesting a regulatory pathway which is no longer needed in invasive carcinoma. The specific AT(1) expression upregulation might well be an important step in the pathogenesis of hyperplasia of the breast, which is regarded as a precursor lesion for breast cancer.
Keywords
breast cancer, hyperplasia, ductal carcinoma in situ, angiotensin II receptor, TAMOXIFEN PREVENTION, CANCER, RISK, PROLIFERATION, INHIBITION, EXPRESSION, FINGERPOST, INSTANCE, DISEASE, TUMORS

Citation

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MLA
De Paepe, Boel, et al. “Growth Stimulatory Angiotensin II Type-1 Receptor Is Upregulated in Breast Hyperplasia and in Situ Carcinoma but Not in Invasive Carcinoma.” HISTOCHEMISTRY AND CELL BIOLOGY, vol. 116, no. 3, 2001, pp. 247–54.
APA
De Paepe, B., Verstraeten, V., De Potter, C., Vakaet, L., & Bullock, G. (2001). Growth stimulatory angiotensin II type-1 receptor is upregulated in breast hyperplasia and in situ carcinoma but not in invasive carcinoma. HISTOCHEMISTRY AND CELL BIOLOGY, 116(3), 247–254.
Chicago author-date
De Paepe, Boel, Valerie Verstraeten, Christian De Potter, Luc Vakaet, and Gillian Bullock. 2001. “Growth Stimulatory Angiotensin II Type-1 Receptor Is Upregulated in Breast Hyperplasia and in Situ Carcinoma but Not in Invasive Carcinoma.” HISTOCHEMISTRY AND CELL BIOLOGY 116 (3): 247–54.
Chicago author-date (all authors)
De Paepe, Boel, Valerie Verstraeten, Christian De Potter, Luc Vakaet, and Gillian Bullock. 2001. “Growth Stimulatory Angiotensin II Type-1 Receptor Is Upregulated in Breast Hyperplasia and in Situ Carcinoma but Not in Invasive Carcinoma.” HISTOCHEMISTRY AND CELL BIOLOGY 116 (3): 247–254.
Vancouver
1.
De Paepe B, Verstraeten V, De Potter C, Vakaet L, Bullock G. Growth stimulatory angiotensin II type-1 receptor is upregulated in breast hyperplasia and in situ carcinoma but not in invasive carcinoma. HISTOCHEMISTRY AND CELL BIOLOGY. 2001;116(3):247–54.
IEEE
[1]
B. De Paepe, V. Verstraeten, C. De Potter, L. Vakaet, and G. Bullock, “Growth stimulatory angiotensin II type-1 receptor is upregulated in breast hyperplasia and in situ carcinoma but not in invasive carcinoma,” HISTOCHEMISTRY AND CELL BIOLOGY, vol. 116, no. 3, pp. 247–254, 2001.
@article{311613,
  abstract     = {{Two different receptors which bind angiotensin II specifically have been identified in humans and were designated angiotensin II type-1 receptor (AT(1)) and angiotensin II type-2 receptor (AT(2)). They only have 34% sequence homology and act through different signalling pathways. AT(1) stimulation has been implicated in hypertrophy and hyperplasia in various tissues. In order to study the involvement of AT(1) in tissues from controls (n=10) and patients with hyperplasia (n=33), ductal carcinoma in situ (DCIS) (n=23) and invasive carcinoma of the breast (n=25), we tested biopsies and breast-derived cell lines using immunocytochemistry, in situ hybridisation and cell proliferation techniques. The results show specific overexpression of AT(1) receptor on the cytoplasmic membrane of cells of hyperplastic lesions with and without atypia and on DCIS of the breast. Evidence for growth stimulation is provided by in vitro experiments showing growth induction by angiotensin II of T47D cells which express the AT(1) but not the AT(2) receptor. The expression of AT(1) on the cell membrane disappears in invasive breast cancer cells suggesting a regulatory pathway which is no longer needed in invasive carcinoma. The specific AT(1) expression upregulation might well be an important step in the pathogenesis of hyperplasia of the breast, which is regarded as a precursor lesion for breast cancer.}},
  author       = {{De Paepe, Boel and Verstraeten, Valerie and De Potter, Christian and Vakaet, Luc and Bullock, Gillian}},
  issn         = {{0948-6143}},
  journal      = {{HISTOCHEMISTRY AND CELL BIOLOGY}},
  keywords     = {{breast cancer,hyperplasia,ductal carcinoma in situ,angiotensin II receptor,TAMOXIFEN PREVENTION,CANCER,RISK,PROLIFERATION,INHIBITION,EXPRESSION,FINGERPOST,INSTANCE,DISEASE,TUMORS}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{247--254}},
  title        = {{Growth stimulatory angiotensin II type-1 receptor is upregulated in breast hyperplasia and in situ carcinoma but not in invasive carcinoma}},
  volume       = {{116}},
  year         = {{2001}},
}
Web of Science
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