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Mutant cell line demonstrating a block in insulin and insulin‐like growth factor type 1 (IGF‐1) induced mitogenesis

Mutant cell line demonstrating a block in insulin and insulin‐like growth factor type 1 (IGF‐1)... 10.1002/jcp.1041550123.abs Recently, we have isolated a Chinese hamster cell variant (IV‐A1‐j) resistant to an insulin‐diphtheria‐A chain toxic conjugate (Leckett and Germinario: Cytotechnology (in press). This cell line exhibited a decreased level of insulin binding, but normal growth in serum‐containing medium when compared to the parental cell line (V‐79). In this paper we further demonstrate that while IV‐A1‐j cells are capable of growing in serum‐containing medium, they are insensitive to the mitogenic actions of either insulin or IGF‐1. In contrast, epidermal growth factor (EGF) and/or α‐thrombin (THR) generate a mitogenic effect in IV‐A1‐j cells comparable to that observed in the parental V‐79 cells. The combination of EGF and/or THR with either insulin or IGF‐1 results in an increase in V‐79 cell growth above EGF and/or THR alone. On the other hand, insulin or IGF‐1 in the presence of other mitogens did not stimulate further growth in IV‐A1‐j cells. While insulin binding was lower in IV‐A1‐j cells, internalization of 125I‐insulin was not different in the two cell types. Additionally, insulin‐stimulated glycogen synthesis and protein synthesis were not different in the two cell types. These observations are consistent with insulin and IGF‐1 sharing a mitogenic signalling pathway in Chinese hamster fibroblasts and that this pathway is distinct from other growth factor signalling pathways. The fact that this pathway is defective in the IV‐A1‐j cell line indicates the potential usefulness of these cells in identifying a key step(s) in the insulin (IGF‐1) mitogenic pathway. © 1993 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Cellular Physiology Wiley

Mutant cell line demonstrating a block in insulin and insulin‐like growth factor type 1 (IGF‐1) induced mitogenesis

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References (36)

Publisher
Wiley
Copyright
Copyright © 1993 Wiley‐Liss, Inc.
ISSN
0021-9541
eISSN
1097-4652
DOI
10.1002/jcp.1041550123
pmid
8468364
Publisher site
See Article on Publisher Site

Abstract

10.1002/jcp.1041550123.abs Recently, we have isolated a Chinese hamster cell variant (IV‐A1‐j) resistant to an insulin‐diphtheria‐A chain toxic conjugate (Leckett and Germinario: Cytotechnology (in press). This cell line exhibited a decreased level of insulin binding, but normal growth in serum‐containing medium when compared to the parental cell line (V‐79). In this paper we further demonstrate that while IV‐A1‐j cells are capable of growing in serum‐containing medium, they are insensitive to the mitogenic actions of either insulin or IGF‐1. In contrast, epidermal growth factor (EGF) and/or α‐thrombin (THR) generate a mitogenic effect in IV‐A1‐j cells comparable to that observed in the parental V‐79 cells. The combination of EGF and/or THR with either insulin or IGF‐1 results in an increase in V‐79 cell growth above EGF and/or THR alone. On the other hand, insulin or IGF‐1 in the presence of other mitogens did not stimulate further growth in IV‐A1‐j cells. While insulin binding was lower in IV‐A1‐j cells, internalization of 125I‐insulin was not different in the two cell types. Additionally, insulin‐stimulated glycogen synthesis and protein synthesis were not different in the two cell types. These observations are consistent with insulin and IGF‐1 sharing a mitogenic signalling pathway in Chinese hamster fibroblasts and that this pathway is distinct from other growth factor signalling pathways. The fact that this pathway is defective in the IV‐A1‐j cell line indicates the potential usefulness of these cells in identifying a key step(s) in the insulin (IGF‐1) mitogenic pathway. © 1993 Wiley‐Liss, Inc.

Journal

Journal of Cellular Physiology – Wiley

Published: Apr 1, 1993

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