Abstract
A high level of estrogen receptor-α (ER-α) is believed to be favorable in the prognosis and treatment of certain female cancers. ER-α expression in the ER-negative breast cancer cell lines inhibits their proliferation and invasive, metastatic potential in vitro. We stably overexpressed the ER-α in the human endometrial cancer cell line Ishikawa and showed that, unlike estradiol, high levels of ER-α significantly inhibit the growth of tumors xenografted from the Ishikawa cells. Subsequent to ER-α overexpression, in vivo down-regulation of vascular endothelial growth factor was observed in tumor xenografts. In addition, these tumors showed an inhibition of vascularization and of the angiogenic agent, integrin αvβ3. Involvement of a switch in the angiogenic pathways during tumorigenesis has been a recent focus of interest. Our results indicate that a high level of ER-α may be beneficial in the control of female cancers because of its inhibitory effect on such angiogenic pathways.
| Original language | English |
|---|---|
| Pages (from-to) | 7094-7098 |
| Number of pages | 5 |
| Journal | Cancer Research |
| Volume | 60 |
| Issue number | 24 |
| Publication status | Published - Dec 15 2000 |
| Externally published | Yes |
Fingerprint
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Estrogen receptor-α in the inhibition of cancer growth and angiogenesis. / Ali, S. H.; O'Donnell, A. L.; Balu, D.; Pohl, M. B.; Seyler, M. J.; Mohamed, S.; Mousa, S.; Dandona, P.
In: Cancer Research, Vol. 60, No. 24, 15.12.2000, p. 7094-7098.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Estrogen receptor-α in the inhibition of cancer growth and angiogenesis
AU - Ali, S. H.
AU - O'Donnell, A. L.
AU - Balu, D.
AU - Pohl, M. B.
AU - Seyler, M. J.
AU - Mohamed, S.
AU - Mousa, S.
AU - Dandona, P.
PY - 2000/12/15
Y1 - 2000/12/15
N2 - A high level of estrogen receptor-α (ER-α) is believed to be favorable in the prognosis and treatment of certain female cancers. ER-α expression in the ER-negative breast cancer cell lines inhibits their proliferation and invasive, metastatic potential in vitro. We stably overexpressed the ER-α in the human endometrial cancer cell line Ishikawa and showed that, unlike estradiol, high levels of ER-α significantly inhibit the growth of tumors xenografted from the Ishikawa cells. Subsequent to ER-α overexpression, in vivo down-regulation of vascular endothelial growth factor was observed in tumor xenografts. In addition, these tumors showed an inhibition of vascularization and of the angiogenic agent, integrin αvβ3. Involvement of a switch in the angiogenic pathways during tumorigenesis has been a recent focus of interest. Our results indicate that a high level of ER-α may be beneficial in the control of female cancers because of its inhibitory effect on such angiogenic pathways.
AB - A high level of estrogen receptor-α (ER-α) is believed to be favorable in the prognosis and treatment of certain female cancers. ER-α expression in the ER-negative breast cancer cell lines inhibits their proliferation and invasive, metastatic potential in vitro. We stably overexpressed the ER-α in the human endometrial cancer cell line Ishikawa and showed that, unlike estradiol, high levels of ER-α significantly inhibit the growth of tumors xenografted from the Ishikawa cells. Subsequent to ER-α overexpression, in vivo down-regulation of vascular endothelial growth factor was observed in tumor xenografts. In addition, these tumors showed an inhibition of vascularization and of the angiogenic agent, integrin αvβ3. Involvement of a switch in the angiogenic pathways during tumorigenesis has been a recent focus of interest. Our results indicate that a high level of ER-α may be beneficial in the control of female cancers because of its inhibitory effect on such angiogenic pathways.
UR - http://www.scopus.com/inward/record.url?scp=0034671391&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034671391&partnerID=8YFLogxK
M3 - Article
VL - 60
SP - 7094
EP - 7098
JO - Journal of Cancer Research
JF - Journal of Cancer Research
SN - 0008-5472
IS - 24
ER -