The fibroblast: growth factor-2 is not essential for melanoma formation in a transgenic mouse model

被引:6
作者
Ackermann, J [1 ]
Beermann, F [1 ]
机构
[1] Swiss Inst Expt Canc Res, NCCR, CH-1066 Epalinges, Switzerland
来源
PIGMENT CELL RESEARCH | 2005年 / 18卷 / 04期
关键词
FGF2; N-ras; knockout; transgenic; melanocyte; tyrosinase;
D O I
10.1111/j.1600-0749.2005.00243.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Fibroblast growth factor 2 (FGF2) has been assigned a role in melanocyte proliferation and in development of human cutaneous melanoma. We have used a transgenic mouse melanoma model in combination with mice lacking mouse FGF2 to analyse the possible implication of FGF2 in melanomagenesis. Tyr::N-ras(Q61K) transgenic mice which are deficient for FGF2 and the tumor suppressors p16(INK4a) and p19(ARF) are hyperpigmented and develop cutaneous metastasizing melanoma, with no difference to mice wildtype for FGF2. We conclude from our data, that FGF2 is not essential for melanoma progression and metastasis.
引用
收藏
页码:315 / 319
页数:5
相关论文
共 33 条
[1]   Metastasizing melanoma formation caused by expression of activated N-RasQ61K on an INK4a-deficient background [J].
Ackermann, J ;
Frutschi, M ;
Kaloulis, K ;
McKee, T ;
Trumpp, A ;
Beermann, F .
CANCER RESEARCH, 2005, 65 (10) :4005-4011
[2]   FGF expression allows nevus cells to survive in three-dimensional collagen gel under conditions that induce apoptosis in normal human melanocytes [J].
Alanko, T ;
Rosenberg, M ;
Saksela, O .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (01) :111-116
[3]   Induction of melanoma phenotypes in human skin by growth factors and ultraviolet B [J].
Berking, C ;
Takemoto, R ;
Satyamoorthy, K ;
Shirakawa, T ;
Eskandarpour, M ;
Hansson, J ;
VanBelle, PA ;
Elder, DE ;
Herlyn, M .
CANCER RESEARCH, 2004, 64 (03) :807-811
[4]   Basic fibroblast growth factor and ultraviolet B transform melanocytes in human skin [J].
Berking, C ;
Takemoto, R ;
Satyamoorthy, K ;
Elenitsas, R ;
Herlyn, M .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (03) :943-953
[5]   Biological roles of fibroblast growth factor-2 [J].
Bikfalvi, A ;
Klein, S ;
Pintucci, G ;
Rifkin, DB .
ENDOCRINE REVIEWS, 1997, 18 (01) :26-45
[6]  
Compagni A, 2000, CANCER RES, V60, P7163
[7]   Mechanisms underlying differential responses to FGF signaling [J].
Dailey, L ;
Ambrosetti, D ;
Mansukhani, A ;
Basilico, C .
CYTOKINE & GROWTH FACTOR REVIEWS, 2005, 16 (02) :233-247
[8]   TRANSFORMATION OF MURINE MELANOCYTES BY BASIC FIBROBLAST GROWTH-FACTOR CDNA AND ONCOGENES AND SELECTIVE SUPPRESSION OF THE TRANSFORMED PHENOTYPE IN A RECONSTITUTED CUTANEOUS ENVIRONMENT [J].
DOTTO, GP ;
MOELLMANN, G ;
GHOSH, S ;
EDWARDS, M ;
HALABAN, R .
JOURNAL OF CELL BIOLOGY, 1989, 109 (06) :3115-3128
[9]   Nuclear localization of mouse fibroblast growth factor 2 requires N-terminal and C-terminal sequences [J].
Foletti, A ;
Vuadens, F ;
Beermann, F .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2003, 60 (10) :2254-2265
[10]   Absence of fibroblast growth factor 2 does not prevent tumor formation originating from the RPE [J].
Foletti, A ;
Ackermann, J ;
Schmidt, A ;
Hummler, E ;
Beermann, F .
ONCOGENE, 2002, 21 (12) :1841-1847