Rap1-suppressed tumorigenesis is concomitant with the interference in Ras effector signaling

Yea Lih Lin; Clément Mettling; Chen Kung Chou

doi:10.1016/S0014-5793(00)01150-9

Rap1-suppressed tumorigenesis is concomitant with the interference in Ras effector signaling

Yea Lih Lin^*, Clément Mettling, Chen Kung Chou

^*Corresponding author for this work

Research output: Contribution to journal › Journal Article › peer-review

6 Scopus citations

Abstract

Expression of Rap1 blocks epithelial growth factor-induced extracellular signal-regulated kinases (ERKs) activation. However, recent studies demonstrated that Rap1 mediates ERKs activation induced by nerve growth factor. The anti-oncogenic effect of Rap1 has been reported but its mechanism remains unclear. To evaluate the correlation between the anti-transforming effect and the activation of ERKs, we transfected rap1 cDNA into Hep3B cells and selected stable transfectants. The Rap1 transfectants completely lost their intrinsic tumorigenicity in Balb/c nude mice. Both insulin and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-stimulated ERK activations were also blocked. Our findings suggest that Rap1-suppressed tumorigenicity is concomitant with ERKs inhibition. Copyright (C) 2000 Federation of European Biochemical Societies.

Original language	English
Pages (from-to)	184-188
Number of pages	5
Journal	FEBS Letters
Volume	467
Issue number	2-3
DOIs	https://doi.org/10.1016/S0014-5793(00)01150-9
State	Published - 11 02 2000
Externally published	Yes

Keywords

12-O-Tetradecanoyl phorbol-13-acetate
Extracellular signal-regulated kinase
GTPase
Insulin
Mitogenesis
Rap1

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10.1016/S0014-5793(00)01150-9

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title = "Rap1-suppressed tumorigenesis is concomitant with the interference in Ras effector signaling",

abstract = "Expression of Rap1 blocks epithelial growth factor-induced extracellular signal-regulated kinases (ERKs) activation. However, recent studies demonstrated that Rap1 mediates ERKs activation induced by nerve growth factor. The anti-oncogenic effect of Rap1 has been reported but its mechanism remains unclear. To evaluate the correlation between the anti-transforming effect and the activation of ERKs, we transfected rap1 cDNA into Hep3B cells and selected stable transfectants. The Rap1 transfectants completely lost their intrinsic tumorigenicity in Balb/c nude mice. Both insulin and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-stimulated ERK activations were also blocked. Our findings suggest that Rap1-suppressed tumorigenicity is concomitant with ERKs inhibition. Copyright (C) 2000 Federation of European Biochemical Societies.",

keywords = "12-O-Tetradecanoyl phorbol-13-acetate, Extracellular signal-regulated kinase, GTPase, Insulin, Mitogenesis, Rap1",

author = "Lin, {Yea Lih} and Cl{\'e}ment Mettling and Chou, {Chen Kung}",

year = "2000",

month = feb,

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doi = "10.1016/S0014-5793(00)01150-9",

language = "英语",

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number = "2-3",

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TY - JOUR

T1 - Rap1-suppressed tumorigenesis is concomitant with the interference in Ras effector signaling

AU - Lin, Yea Lih

AU - Mettling, Clément

AU - Chou, Chen Kung

PY - 2000/2/11

Y1 - 2000/2/11

N2 - Expression of Rap1 blocks epithelial growth factor-induced extracellular signal-regulated kinases (ERKs) activation. However, recent studies demonstrated that Rap1 mediates ERKs activation induced by nerve growth factor. The anti-oncogenic effect of Rap1 has been reported but its mechanism remains unclear. To evaluate the correlation between the anti-transforming effect and the activation of ERKs, we transfected rap1 cDNA into Hep3B cells and selected stable transfectants. The Rap1 transfectants completely lost their intrinsic tumorigenicity in Balb/c nude mice. Both insulin and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-stimulated ERK activations were also blocked. Our findings suggest that Rap1-suppressed tumorigenicity is concomitant with ERKs inhibition. Copyright (C) 2000 Federation of European Biochemical Societies.

AB - Expression of Rap1 blocks epithelial growth factor-induced extracellular signal-regulated kinases (ERKs) activation. However, recent studies demonstrated that Rap1 mediates ERKs activation induced by nerve growth factor. The anti-oncogenic effect of Rap1 has been reported but its mechanism remains unclear. To evaluate the correlation between the anti-transforming effect and the activation of ERKs, we transfected rap1 cDNA into Hep3B cells and selected stable transfectants. The Rap1 transfectants completely lost their intrinsic tumorigenicity in Balb/c nude mice. Both insulin and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-stimulated ERK activations were also blocked. Our findings suggest that Rap1-suppressed tumorigenicity is concomitant with ERKs inhibition. Copyright (C) 2000 Federation of European Biochemical Societies.

KW - 12-O-Tetradecanoyl phorbol-13-acetate

KW - Extracellular signal-regulated kinase

KW - GTPase

KW - Insulin

KW - Mitogenesis

KW - Rap1

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ER -

Rap1-suppressed tumorigenesis is concomitant with the interference in Ras effector signaling

Abstract

Keywords

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