Cripto enhances the tyrosine phosphorylation of Shc and activates mitogen-activated protein kinase (MAPK) in mammary epithelial cells

被引:94
作者
Kannan, S
DeSantis, M
Lohmeyer, M
Riese, DJ
Smith, GH
Hynes, N
Seno, M
Brandt, R
Bianco, C
Persico, G
Kenney, N
Normanno, N
MartinezLacaci, I
Ciardiello, F
Stern, DF
Gullick, WJ
Salomon, DS
机构
[1] NCI,TUMOR IMMUNOL & BIOL LAB,TUMOR GROWTH FACTOR SECT,NIH,BETHESDA,MD 20892
[2] HAMMERSMITH HOSP,ICRF ONCOL UNIT,LONDON,ENGLAND
[3] YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06520
[4] FRIEDRICH MIESCHER INST,CH-4002 BASEL,SWITZERLAND
[5] IST INT GENET & BIOFIS,NAPLES,ITALY
[6] GEORGETOWN UNIV,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007
[7] UNIV NAPLES,FAC MED & CHIRURG 2,CATTEDRA ONCOL MED 2,I-80131 NAPLES,ITALY
关键词
D O I
10.1074/jbc.272.6.3330
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cripto-1 (CR-1), a recently discovered protein of the epidermal growth factor (EGF) family; was found to interact with a high affinity, saturable binding site(s) on HC-11 mouse mammary epithelial cells and on several different human breast cancer cell lines. This receptor exhibits specificity for CR-1, since other EGF-related peptides including EGF, transforming growth factor cu, heparin-binding EGF-like growth factor, amphiregulin, epiregulin, betacellulin, or heregulin beta 1 that bind to either the EGF receptor or to other type 1 receptor tyrosine kinases such as erb B-3 or erb B-4 fail to compete for binding, Conversely, CR-1 was found not to directly bind to or to activate the tyrosine kinases associated with Shc EGFR, erb B-2, erb B-3, or erb B-4 either alone or in various pairwise combinations which have been ectopically expressed in Ba/F3 mouse pro-B lymphocyte cells. However, exogenous CR-1 could induce an increase in the tyrosine phosphorylation of 185- and 120-kDa proteins and a rapid (within 3-5 min) increase in the tyrosine phosphorylation of the SH2-containing adaptor proteins p66, p52, and p46 She in mouse mammary HC-11 epithelial cells and in human MDA-MB-453 and SKBr-3 breast cancer cells. CR-1 was also found to promote an increase in the association of the adaptor Grb2-guanine nucleotide exchange factor-mouse son of sevenless (mSOS) signaling complex with tyrosine-phosphorylated She in HC-11 cells. Finally, CR-1 was able to increase p42(erk-2) mitogen-activated protein kinase (MAPK) activity in HC-11 cells within 5-10 min of treatment. These data demonstrate that CR-1 can function through a receptor which activates intracellular components in the ras/raf/MEK/MAPK pathway.
引用
收藏
页码:3330 / 3335
页数:6
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