Osteopontin expression correlates with melanoma invasion

被引:18
作者
Denhardt, D [1 ]
机构
[1] Rutgers State Univ, Nelson Biol Labs, Dept Cell Biol & Neurosci, Piscataway, NJ 08855 USA
[2] Rutgers State Univ, Nelson Biol Labs, Canc Inst New Jersey, Piscataway, NJ USA
基金
加拿大创新基金会; 加拿大健康研究院;
关键词
D O I
10.1111/j.0022-202X.2005.23708.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Melanoma is one of the most aggressive cancers affecting humans. Although early melanomas are curable with surgical excision, metastatic melanomas are associated with high mortality. The mechanism of melanoma development, progression, and metastasis is largely unknown. In order to uncover genes unique to melanoma cells, we used high-density DNA microarrays to examine the gene expression profiles of metastatic melanoma nodules using benign nevi as controls. Over 190 genes were significantly overexpressed in metastatic melanomas compared with normal nevi by at least 2-fold. One of the most abundantly expressed genes in metastatic melanoma nodules is osteopontin (OPN). Immunohistochemistry staining on tissue microarrays and individual skin biopsies representing different stages of melanoma progression revealed that OPN expression is first acquired at the step of melanoma tissue invasion. In addition, blocking of OPN expression by RNA interference reduced melanoma cell numbers in vitro. Our observations suggest that OPN may be acquired early in melanoma development and progression, and may enhance tumor cell growth in invasive melanoma. Copyright © 2005 by The Society for Investigative Dermatology, Inc.
引用
收藏
页码:XVI / XVIII
页数:3
相关论文
共 27 条
[1]   Downregulation of osteopontin and bone sialoprotein II is related to reduced colony formation and metastasis formation of MDA-MB-231 human breast cancer cells [J].
Adwan, H ;
Bäuerle, TJ ;
Berger, MR .
CANCER GENE THERAPY, 2004, 11 (02) :109-120
[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]   Osteopontin contributes to hepatocyte growth factor-induced tumor growth and metastasis formation [J].
Ariztia, EV ;
Subbarao, V ;
Solt, DB ;
Rademaker, AW ;
Iyer, AP ;
Oltvai, ZN .
EXPERIMENTAL CELL RESEARCH, 2003, 288 (02) :257-267
[4]   Correlation of osteopontin protein expression and pathological stage across a wide variety of tumor histologies [J].
Coppola, D ;
Szabo, M ;
Boulware, D ;
Muraca, P ;
Alsarraj, M ;
Chambers, AF ;
Yeatman, TJ .
CLINICAL CANCER RESEARCH, 2004, 10 (01) :184-190
[5]   Transcriptional regulation of osteopontin and the metastatic phenotype: Evidence for a Ras-activated enhancer in the human OPN promoter [J].
Denhardt, DT ;
Mistretta, D ;
Chambers, AF ;
Krishna, S ;
Porter, JF ;
Raghuram, S ;
Rittling, SR .
CLINICAL & EXPERIMENTAL METASTASIS, 2003, 20 (01) :77-84
[6]   Role of osteopontin in cellular signaling and toxicant injury [J].
Denhardt, DT ;
Giachelli, CM ;
Rittling, SR .
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, 2001, 41 :723-749
[7]   Osteopontin as a means to cope with environmental insults: regulation of inflammation, tissue remodeling, and cell survival [J].
Denhardt, DT ;
Noda, M ;
O'Regan, AW ;
Pavlin, D ;
Berman, JS .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (09) :1055-1061
[8]   Three small integrin-binding ligand N-linked glycoproteins (SIBLINGs) bind and activate specific matrix metalloproteinases [J].
Fedarko, NS ;
Jain, A ;
Karadag, A ;
Fisher, LW .
FASEB JOURNAL, 2004, 18 (02) :734-+
[9]  
Furger Kara A., 2001, Current Molecular Medicine (Hilversum), V1, P621, DOI 10.2174/1566524013363339
[10]  
Geissinger E, 2002, CANCER RES, V62, P4820