Insulin-like growth factor II stimulates cell proliferation through the insulin receptor.
R- cells are 3T3-like fibroblasts generated from mouse embryos nullizygous for a targeted disruption of the genes encoding the type 1 insulin-like growth factor (IGF) receptor (IGF1R). These cells fail to proliferate in serum-free medium supplemented with purified growth factors, in contrast to their wild-type counterparts. However, when R- cells overexpress the insulin receptor from a stably integrated plasmid, R-/IR cells, they become capable of growing in serum-free medium supplemented solely with insulin or IGF-II, but not with IGF-I. Moreover, the introduction into R-/IR cells of an additional plasmid expressing IGF-II causes these cells to proliferate in serum-free medium without growth factor supplementation. From these results, we conclude that IGF-II can stimulate cell proliferation not only through its cognate IGF1R but also through the insulin receptor.
Morrione
A
A
Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107-5541, USA.
Valentinis
B
B
Xu
S Q
SQ
Yumet
G
G
Louvi
A
A
Efstratiadis
A
A
Baserga
R
R
D016475:3T3 Cells; D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D006801:Humans; D007335:Insulin-Like Growth Factor II / Q000378:metabolism / Q000494:pharmacology*; D051379:Mice; D010957:Plasmids; D011972:Receptor, Insulin / Q000819:agonists* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D014162:Transfection
D007335:Insulin-Like Growth Factor II; D011972:Receptor, Insulin