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Influence of IGF-IR stimulation or blockade on proliferation of human renal cell carcinoma cell lines

Rosendahl, Ann LU and Forsberg, G (2004) In International Journal of Oncology 25(5). p.1327-1336
Abstract
Several tumors secrete insulin-like growth factors (IGFs) for autocrine growth stimulation and protection from apoptosis. However, the mechanisms responsible for tumor growth in renal cell carcinoma (RCC) are unclear. In this study the biological role of exogenous IGFs in two malignant RCC cells (Caki-2 and SK-RC-52) were investigated in vitro, and compared to the breast cancer cell line MCF-7. IGFs but not the related epidermal growth factor stimulated both RCC cell lines. Caki-2 expressed higher levels of IGF-IR and proliferated more vigorously to added IGF-I, IGF-I analogues des(1-3)IGF-I, LongR(3)IGF-I and IGF-II compared to SK-RC-52. Neutralizing IGF-IR antibodies reduced the IGF driven proliferation in both cell lines. Interestingly,... (More)
Several tumors secrete insulin-like growth factors (IGFs) for autocrine growth stimulation and protection from apoptosis. However, the mechanisms responsible for tumor growth in renal cell carcinoma (RCC) are unclear. In this study the biological role of exogenous IGFs in two malignant RCC cells (Caki-2 and SK-RC-52) were investigated in vitro, and compared to the breast cancer cell line MCF-7. IGFs but not the related epidermal growth factor stimulated both RCC cell lines. Caki-2 expressed higher levels of IGF-IR and proliferated more vigorously to added IGF-I, IGF-I analogues des(1-3)IGF-I, LongR(3)IGF-I and IGF-II compared to SK-RC-52. Neutralizing IGF-IR antibodies reduced the IGF driven proliferation in both cell lines. Interestingly, soluble IGF-I receptor resulted in strong growth inhibition of SK-RC-52, while no marked effect on Caki-2 was observed. Moreover, Caki-2 expressed a broad panel of IGFBPs, while SK-RC-52 more selectively secreted high levels of IGFBP-3. Exogenous IGFBP-3 strongly inhibited IGF-I driven proliferation in SK-RC-52, but worked in synergy with IGF-I in Caki-2. Both the IGF-IR and IGFBP-3 were present in respectively 4/4 and 4/8 human malignant renal tissues. In light of this and with the functional data presented in this study, interference with this growth factor system may provide a novel therapeutic approach in renal cancer therapy. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
renal cancer, insulin-like growth factor, analogues, soluble receptor, proliferation
in
International Journal of Oncology
volume
25
issue
5
pages
1327 - 1336
publisher
D.A. Spandidos
external identifiers
  • wos:000224713500015
  • pmid:15492822
  • scopus:16644387550
ISSN
1019-6439
language
English
LU publication?
yes
id
edc39b9a-4dcb-40e5-a1f8-a8fbb94bea51 (old id 262434)
date added to LUP
2007-10-31 09:39:44
date last changed
2017-01-01 07:23:04
@article{edc39b9a-4dcb-40e5-a1f8-a8fbb94bea51,
  abstract     = {Several tumors secrete insulin-like growth factors (IGFs) for autocrine growth stimulation and protection from apoptosis. However, the mechanisms responsible for tumor growth in renal cell carcinoma (RCC) are unclear. In this study the biological role of exogenous IGFs in two malignant RCC cells (Caki-2 and SK-RC-52) were investigated in vitro, and compared to the breast cancer cell line MCF-7. IGFs but not the related epidermal growth factor stimulated both RCC cell lines. Caki-2 expressed higher levels of IGF-IR and proliferated more vigorously to added IGF-I, IGF-I analogues des(1-3)IGF-I, LongR(3)IGF-I and IGF-II compared to SK-RC-52. Neutralizing IGF-IR antibodies reduced the IGF driven proliferation in both cell lines. Interestingly, soluble IGF-I receptor resulted in strong growth inhibition of SK-RC-52, while no marked effect on Caki-2 was observed. Moreover, Caki-2 expressed a broad panel of IGFBPs, while SK-RC-52 more selectively secreted high levels of IGFBP-3. Exogenous IGFBP-3 strongly inhibited IGF-I driven proliferation in SK-RC-52, but worked in synergy with IGF-I in Caki-2. Both the IGF-IR and IGFBP-3 were present in respectively 4/4 and 4/8 human malignant renal tissues. In light of this and with the functional data presented in this study, interference with this growth factor system may provide a novel therapeutic approach in renal cancer therapy.},
  author       = {Rosendahl, Ann and Forsberg, G},
  issn         = {1019-6439},
  keyword      = {renal cancer,insulin-like growth factor,analogues,soluble receptor,proliferation},
  language     = {eng},
  number       = {5},
  pages        = {1327--1336},
  publisher    = {D.A. Spandidos},
  series       = {International Journal of Oncology},
  title        = {Influence of IGF-IR stimulation or blockade on proliferation of human renal cell carcinoma cell lines},
  volume       = {25},
  year         = {2004},
}