HGF and c-MET as potential orchestrators of invasive growth in head and neck squamous cell carcinoma

被引:44
作者
De Herdt, Maria-Jantine [1 ]
de Jong, Robert J. Baatenburg [1 ]
机构
[1] Univ Med Ctr Rotterdam, Erasmus MC, Dept Otolaryngol & Head & Neck Surg, NL-3000 CA Rotterdam, Netherlands
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2008年 / 13卷
关键词
HNSCC; invasive growth; metastasis; epithelial; mesenchymal; ECM; cell-cell dissociation; EMT; proteolysis of the ECM; migration; anoikis; signaling; HGF; c-MET; E-cadherin; ERK; Egr1; Snail; E1AF; MMP1; MMP2; MMP3; MMP9; MMP14; RHOA; RAC1; CDC42; collagen type I; collagen type IV; integrin-beta1; alpha-actinin; vinculin; tensin; paxillin; c-SRC; FAK; Akt; AP-1; c-Jun; c-Fos; Cox-2; IL8; VEGF; PDGFA; review;
D O I
10.2741/2863
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
Head and neck squamous cell carcinoma (HNSCC) constitutes 90% of all head and neck cancers and is associated with high mortality rates, due to the high infiltrative potential of these tumors. Despite advances in treatment approaches, there has been no improvement in survival rates. As empiricism in the treatment of HNSCC is unlikely to improve the prognosis of HNSCC patients, understanding the pathogenesis behind the local invasion of these tumors on the cellular and molecular levels has become an important goal in the field of head and neck surgery. It is believed that the invasive growth of neoplastic cells is a deregulated form of the physiological program that occurs during the formation and patterning of an embryo, which is largely facilitated by HGF induced signaling through its receptor c-MET. T his review investigates whether HGF and c-MET are deregulated in HNSCC and whether they confer an invasive potential to these tumors. It is concluded that both molecules are mis-and over-expressed in HNSCC and probably induce the program of invasive growth in HNSCC.
引用
收藏
页码:2516 / 2526
页数:11
相关论文
共 76 条
[1]   Metalloproteinase expression in normal and malignant oral keratinocytes: stimulation of MMP-2 and-9 by scatter factor [J].
Bennett, JH ;
Morgan, MJ ;
Whawell, SA ;
Atkin, P ;
Roblin, P ;
Furness, J ;
Speight, PM .
EUROPEAN JOURNAL OF ORAL SCIENCES, 2000, 108 (04) :281-291
[2]   Tyrosine kinase signal specificity: lessons from the HGF receptor [J].
Bertotti, A ;
Comoglio, PM .
TRENDS IN BIOCHEMICAL SCIENCES, 2003, 28 (10) :527-533
[3]   Developmental roles of HGF/SF and its receptor, the c-Met tyrosine kinase [J].
Birchmeier, C ;
Gherardi, E .
TRENDS IN CELL BIOLOGY, 1998, 8 (10) :404-410
[4]   Met, metastasis, motility and more [J].
Birchmeier, C ;
Birchmeier, W ;
Gherardi, E ;
Vande Woude, GF .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2003, 4 (12) :915-925
[5]   Opinion -: Invasive growth:: a MET-driven genetic programme for cancer and stem cells [J].
Boccaccio, Carla ;
Comoglio, Paolo M. .
NATURE REVIEWS CANCER, 2006, 6 (08) :637-645
[6]   Epithelial cell shape: Cadherins and small GTPases [J].
Braga, V .
EXPERIMENTAL CELL RESEARCH, 2000, 261 (01) :83-90
[7]   The transcription factor Snail controls epithelial-mesenchymal transitions by repressing E-cadherin expression [J].
Cano, A ;
Pérez-Moreno, MA ;
Rodrigo, I ;
Locascio, A ;
Blanco, MJ ;
del Barrio, MG ;
Portillo, F ;
Nieto, MA .
NATURE CELL BIOLOGY, 2000, 2 (02) :76-83
[8]   Cell adhesion and signalling by cadherins and Ig-CAMs in cancer [J].
Cavallaro, U ;
Christofori, G .
NATURE REVIEWS CANCER, 2004, 4 (02) :118-132
[9]   Expression of hepatocyte growth factor and c-met protein is significantly associated with the progression of oral squamous cell carcinoma in Taiwan [J].
Chen, YS ;
Wang, JT ;
Chang, YF ;
Liu, BY ;
Wang, YP ;
Sun, A ;
Chiang, CP .
JOURNAL OF ORAL PATHOLOGY & MEDICINE, 2004, 33 (04) :209-217
[10]   Cancer therapy: can the challenge be MET? [J].
Corso, S ;
Comoglio, PM ;
Giordano, S .
TRENDS IN MOLECULAR MEDICINE, 2005, 11 (06) :284-292