Influence of IGF-IR stimulation or blockade on proliferation of human renal cell carcinoma cell lines
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/262434
- author
- Rosendahl, Ann LU and Forsberg, G
- organization
- publishing date
- 2004
- 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
- Spandidos Publications
- 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
- 2016-04-01 17:03:33
- date last changed
- 2022-01-29 00:01:06
@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}},
keywords = {{renal cancer; insulin-like growth factor; analogues; soluble receptor; proliferation}},
language = {{eng}},
number = {{5}},
pages = {{1327--1336}},
publisher = {{Spandidos Publications}},
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}},
}