Distribution of SPARC in normal and neoplastic human                tissue.

Porter, Peggy L.; Sage, E. Helene; Lane, Timothy F.; Funk, Sarah E.; Gown, Allen M.

doi:10.1177/43.8.7622842

Cited by 187 publications

(149 citation statements)

References 12 publications

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“…17 SPARC overexpression has previously been associated with human tumors. 20 Porte et al 21 identified an association of SPARC with colorectal carcinoma, where neoplastic progression was associated with overexpression of the stromelysin-3 and SPARC genes. Massi et al 22 demonstrated in 188 patients with thin (Ͻ0.75 mm) melanoma that SPARC positivity on IHC staining correlated with significantly poorer survival.…”

Section: Discussionmentioning

confidence: 99%

Novel markers for poor prognosis in head and neck cancer

Chin

Boyle

Williams

et al. 2004

Intl Journal of Cancer

147

111

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Head and neck cancer (HNSCC) is one of the most distressing human cancers, causing pain and affecting the basic survival functions of breathing and swallowing. Mortality rates have not changed despite recent advances in radiotherapy and surgical treatment. We have compared the expression of over 13,000 unique genes in 7 cases of matched HNSCC and normal oral mucosa. Of the 1,260 genes that showed statistically significant differences in expression between normal and tumor tissue at the mRNA level, the three top ranking of the top 5% were selected for further analysis by immunohistochemistry on paraffin sections, along with the tumor suppressor genes p16 and p53, in a total of 62 patients including 55 for whom >4-year clinical data was available. Using univariate and multivariate survival analysis, we identified SPARC/osteonectin as a powerful independent prognostic marker for short disease-free interval (DFI) (p < 0.002) and poor overall survival (OS) (p ‫؍‬ 0.018) of HNSCC patients. In combination with other ECM proteins found in our analysis, PAI-1 and uPA, the association with DFI and OS became even more significant (p < 0.001). Our study represents the first instance of SPARC as an independent prognostic marker in HNSCC.

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Section: Discussionmentioning

confidence: 99%

Novel markers for poor prognosis in head and neck cancer

Chin

Boyle

Williams

et al. 2004

Intl Journal of Cancer

147

111

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show abstract

“…It is a 43-kDa secreted extracellular glycoprotein that has important roles in development, tissue healing, remodeling and angiogenesis (Bradshaw and Sage, 2001;Framson and Sage, 2004). SPARC is expressed in epithelia exhibiting high rates of turnover (Sage et al, 1989;Porter et al, 1995). It is able to induce an intermediate stage of cellular adhesion with ablation of focal adhesions, to regulate matrix deposition and to induce growth inhibition in different cancer cells (Murphy-Ullrich et al, 1995;Bradshaw and Sage, 2001;Framson and Sage, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…In addition to its physiological role, SPARC has been linked to cancer progression as many cancer types present increased levels of SPARC expression upon invasion or metastasis (Rempel et al, 1998;Loging et al, 2000;Bradshaw and Sage, 2001;Framson and Sage, 2004). SPARC is highly expressed in a wide range of human malignant neoplasms, and the deregulated expression of SPARC is often correlated with disease progression and/or poor prognosis (Bellahcene and Castronovo, 1995;Porte et al, 1995Porte et al, , 1998Porter et al, 1995;Massi et al, 1999;Yamanaka et al, 2001). It can interact with different ECM proteins like collagens, matrix metalloproteinases and growth factors modulating the cell shape, growth, adhesion and migration.…”

Section: Introductionmentioning

confidence: 99%

TP53INP1 decreases pancreatic cancer cell migration by regulating SPARC expression

et al. 2011

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Tumor protein 53 induced nuclear protein 1 (TP53INP1) is a p53 target gene that induces cell growth arrest and apoptosis by modulating p53 transcriptional activity. TP53INP1 interacts physically with p53 and is a major player in the p53-driven oxidative stress response. Previously, we demonstrated that TP53INP1 is downregulated in an early stage of pancreatic cancerogenesis and when restored is able to suppress pancreatic tumor development. TP53INP1 downregulation in pancreas is associated with an oncogenic microRNA miR-155. In the present work, we studied the effects of TP53INP1 on cell migration. We found that TP53INP1 inactivation correlates with increased cell migration both in vivo and in vitro. The impact of TP53INP1 expression on cell migration was studied in different cellular contexts: mouse embryonic fibroblast and different pancreatic cancer cell lines. Its expression decreases cell migration by the transcriptional downregulation of secreted protein acidic and rich in cysteine (SPARC). SPARC is a matrix cellular protein, which governs diverse cellular functions and has a pivotal role in regulating cell-matrix interactions, cellular proliferation and migration. SPARC was also showed to be upregulated in normal pancreas and in pancreatic intraepithelial neoplasia lesions in a pancreatic adenocarcinoma mouse model only in the TP53INP1-deficient animals. This novel TP53INP1 activity on the regulation of SPARC expression could explain in part its tumor suppressor function in pancreatic adenocarcinoma by modulating cellular spreading during the metastatic process.

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“…SPARC is highly expressed during embryogenesis, and its expression becomes more restricted in adult tissues (2). It is highly expressed in adult bone tissues and during processes involving tissue remodeling such as tumorigenesis and wound repair.…”

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confidence: 99%

The Novel SPARC Family Member SMOC-2 Potentiates Angiogenic Growth Factor Activity

Rocnik

Liu

Sato

et al. 2006

Journal of Biological Chemistry

106

109

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SMOC-2 is a novel member of the SPARC family of matricellular proteins. The purpose of this study was to determine whether SMOC-2 can modulate angiogenic growth factor activity and angiogenesis. SMOC-2 was localized in the extracellular periphery of cultured human umbilical vein endothelial cells (HUVECs). Ectopically expressed SMOC-2 was also secreted into the tissue culture medium. In microarray profiling experiments, a recombinant SMOC-2 adenovirus induced the expression of transcripts required for cell cycle progression in HUVECs. Consistent with a growth-stimulatory role for SMOC-2, its overexpression stimulated DNA synthesis in a dosedependent manner. Overexpressed SMOC-2 also synergized with vascular endothelial growth factor or with basic fibroblast growth factor to stimulate DNA synthesis. Ectopically expressed SMOC-2 stimulated formation of network-like structures as determined by in vitro matrigel angiogenesis assays. Fetal calf serum enhanced the stimulatory effect of overexpressed SMOC-2 in this assay. Conversely, small interference RNA directed toward SMOC-2 inhibited network formation and proliferation. The angiogenic activity of SMOC-2 was also examined in experimental mice by subdermal implantation of Matrigel plugs containing SMOC-2 adenovirus. SMOC-2 adenovirus induced a 3-fold increase in the number of cells invading Matrigel plugs when compared with a control adenoviral vector. Basic fibroblast growth factor and SMOC-2 elicited a synergistic effect on cell invasion. Taken together, our results demonstrate that SMOC-2 is a novel angiogenic factor that potentiates angiogenic effects of growth factors.

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Distribution of SPARC in normal and neoplastic human tissue.

Cited by 187 publications

References 12 publications

Novel markers for poor prognosis in head and neck cancer

Novel markers for poor prognosis in head and neck cancer

TP53INP1 decreases pancreatic cancer cell migration by regulating SPARC expression

The Novel SPARC Family Member SMOC-2 Potentiates Angiogenic Growth Factor Activity

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