Paths of FGFR-driven tumorigenesis

被引：132

作者：

Acevedo, Victor D. ^{[1
,2
]}

Ittmann, Michael ^{[3
]}

Spencer, David M. ^{[1
,2
]}

机构：

[1] Baylor Coll Med, Cell & Mol Biol Program, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA

[3] Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA

来源：

CELL CYCLE | 2009年 / 8卷 / 04期

关键词：

prostate cancer; fibroblast growth factor receptor (FGFR); chemical inducer of dimerization (CID); epithelial-mesenchymal transition (EMT); angiogenesis; androgen independence; FIBROBLAST-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; RECEPTOR TYROSINE KINASE; PROSTATE-CANCER; ANDROGEN-RECEPTOR; TUMOR-GROWTH; ENDOTHELIAL-CELLS; INTRAEPITHELIAL NEOPLASIA; TRANSCRIPTION FACTOR; STRUCTURAL BASIS;

D O I：

10.4161/cc.8.4.7657

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Fibroblast growth factor receptors (FGFRs) comprise a subfamily of receptor tyrosine kinases (RTKs) that are master regulators of a broad spectrum of cellular and developmental processes, including apoptosis, proliferation, migration and angiogenesis. Due to their broad impact, FGFRs and other RTKs are highly regulated and normally only basally active. Deregulation of FGFR signaling by activating mutations or ligand/receptor overexpression could allow these receptors to become constitutively active, leading to cancer development, including both hematopoietic and solid tumors, such as breast, bladder and prostate carcinomas. In this review, we focus on potential modes of FGFR-mediated tumorigenesis, in particular, the role of FGFR1 during prostate cancer progression.

引用

页码：580 / 588

页数：9

共 123 条

[81] In vivo and in vitro evidence for transforming growth factor-β1-mediated epithelial to mesenchymal transition in esophageal adenocarcinoma
Rees, Jonathan R. E.
Onwuegbusi, Benjamin A.
Save, Vicki E.
Alderson, Derek
Fitzgerald, Rebecca C.
[J]. CANCER RESEARCH, 2006, 66 (19) : 9583 - 9590
[82] Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations
Roumiantsev, S
Krause, DS
Neumann, CA
Dimitri, CA
Asiedu, F
Cross, NCP
Van Etten, RA
[J]. CANCER CELL, 2004, 5 (03) : 287 - 298
[83] Selective over-expression of fibroblast growth factor receptors 1 and 4 in clinical prostate cancer
Sahadevan, K.
Darby, S.
Leung, H. Y.
Mathers, M. E.
Robson, C. N.
Gnanapragasam, V. J.
[J]. JOURNAL OF PATHOLOGY, 2007, 213 (01) : 82 - 90
[84] Cooperative action of Sox9, Snail2 and PKA signaling in early neural crest development
Sakai, D
Suzuki, T
Osumi, N
Wakamatsu, Y
[J]. DEVELOPMENT, 2006, 133 (07): : 1323 - 1333
[85] Src kinase modulates the activation, transport and signalling dynamics of fibroblast growth factor receptors
Sandilands, Emma
Akbarzadeh, Shiva
Vecchione, Anna
McEwan, David G.
Frame, Margaret C.
Heath, John K.
[J]. EMBO REPORTS, 2007, 8 (12) : 1162 - 1169
[86] Mammalian Sprouty4 suppresses Ras-independent ERK activation by binding to Raf1
Sasaki, A
Taketomi, T
Kato, R
Saeki, K
Nonami, A
Sasaki, M
Kuriyama, M
Saito, N
Shibuya, M
Yoshimura, A
[J]. NATURE CELL BIOLOGY, 2003, 5 (05) : 427 - 432
[87] ALTERNATIVE SPLICING IN FIBROBLAST GROWTH-FACTOR RECEPTOR-2 IS ASSOCIATED WITH INDUCED EPITHELIAL-MESENCHYMAL TRANSITION IN RAT BLADDER-CARCINOMA CELLS
SAVAGNER, P
VALLES, AM
JOUANNEAU, J
YAMADA, KM
THIERY, JP
[J]. MOLECULAR BIOLOGY OF THE CELL, 1994, 5 (08) : 851 - 862
[88] The zinc-finger protein slug causes desmosome dissociation, an initial and necessary step for growth factor-induced epithelial-mesenchymal transition
Savagner, P
Yamada, KM
Thiery, JP
[J]. JOURNAL OF CELL BIOLOGY, 1997, 137 (06) : 1403 - 1419
[89] Cell Signaling by Receptor Tyrosine Kinases
Lemmon, Mark A.
Schlessinger, Joseph
[J]. CELL, 2010, 141 (07) : 1117 - 1134
[90] A critical role for the inflammatory response in a mouse model of preneoplastic progression
Schwertfeger, Kathryn L.
Xian, Wa
Kaplan, Alan M.
Burnett, Sandra H.
Cohen, Donald A.
Rosen, Jeffrey M.
[J]. CANCER RESEARCH, 2006, 66 (11) : 5676 - 5685

← 4 5 6 7 8 9 10 11 12 13 →