Testican-1: A Differentially Expressed Proteoglycan with Protease Inhibiting Activities

Edgell, Cora‐Jean S.; BaSalamah, Mohammad A.; Marr, Henry S.

doi:10.1016/s0074-7696(04)36003-1

Cited by 47 publications

(36 citation statements)

References 37 publications

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“…Similar findings have been briefly reported, but not documented, in a recent review article (Edgell et al, 2004). In the assumption that the apparent lack of phenotype is due to a functional redundancy among the members of the BM-40/SPARC/osteonectin protein family, we determined the expression of testican-2, testican-3 and SC1/hevin in testican-1 deficient mouse brains, but failed to find any evidence for an upregulation.…”

Section: Discussionsupporting

confidence: 84%

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Testican-1 is dispensable for mouse development

et al. 2006

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Section: Discussionsupporting

confidence: 84%

“…In contrast, the human expression is much broader, with testican-1 found, not only in brain, but also in e.g. prostate, testicle, heart, blood and cartilage (Marr et al, 1997;BaSalamah et al, 2001;Edgell et al, 2004;Hausser et al, 2004).…”

Section: Introductionmentioning

confidence: 98%

Testican-1 is dispensable for mouse development

et al. 2006

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“…Similarly, recent studies have shown that SPOCK1 is also involved in such diverse activities. SPOCK1 has an inhibitory role in protease activities and cell attachment [58][59][60]. Moreover, SPOCK1 is involved in TGF-β1 signaling and regulates the epithelial-mesenchymal transition [61].…”

Section: Discussionmentioning

confidence: 99%

Plakophilin 1-deficient cells upregulate SPOCK1: implications for prostate cancer progression

et al. 2015

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Plakophilin (PKP) 1 is frequently downregulated in prostate cancer and therefore may play a tumor-suppressive role. In the present study, we stably knocked down PKP1 in the non-neoplastic, prostatic BPH-1 cell line. In the PKP1-deficient cells, the expression of keratin 14 was lost, and the apoptosis rate was significantly reduced indicating that the cells acquired new biological capabilities. Moreover, we analyzed the gene expression profile of the PKP1-deficient BPH-1 cells. Among the genes that were significantly altered upon PKP1 knockdown, we noticed several extracellular matrix (ECM)-related genes and identified sparc/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1/testican-1) as a gene of interest. SPOCK1 is a component of the ECM and belongs to a matricellular protein family named secreted protein, acidic, cysteine-rich (SPARC). The role of SPOCK1 in prostate cancer has not been clearly elucidated. We analyzed SPOCK1 mRNA expression levels in different cancer databases and characterized its expression in 136 prostatic adenocarcinomas by immunohistochemistry and western blot. SPOCK1 revealed a cytoplasmic localization in the glandular epithelium of the prostate and showed a significant upregulation of mRNA and protein in prostate tumor samples. Our findings support the hypothesis that PKP1 may have a tumor-suppressive function and suggest an important role of SPOCK1 in prostate tumor progression. Collectively, altered expression of PKP1 and SPOCK1 appears to be a frequent and critical event in prostate cancer.

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“…The purified gene product has been shown to inhibit cell attachment and neurite extension in culture and to inhibit membrane type 1 and 2 matrix metalloproteinases (Edgell et al, 2004). It remains to be determined whether SPOCK1 expressed by PA contributes to their noninvasive behavior.…”

Section: Discussionmentioning

confidence: 99%

Identification of genes differentially expressed in glioblastoma versus pilocytic astrocytoma using Suppression Subtractive Hybridization

et al. 2005

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Glioblastoma (GBM) is a highly malignant glioma, which has the propensity to infiltrate throughout the brain in contrast to pilocytic astrocytoma (PA) of the posterior fossa, which does not spread and can be cured by surgery. We have used Suppression Subtractive Hybridization to define markers that better delineate the molecular basis of brain invasion and distinguish these tumor groups. We have identified 106 genes expressed in PA versus GBM and 80 genes expressed in GBM versus PA. Subsequent analysis identified a subset of 20 transcripts showing a common differential expression pattern for the two groups. GBM differs from PA by the expression of five genes involved in invasion and angiogenesis: fibronectin, osteopontin, chitinase-3-like-1 (YKL-40), keratoepithelin and fibromodulin. PA differs from GBM by the expression of genes related to metabolism (apolipoprotein D), proteolysis (protease-serine-11), receptor and signal transduction (PLEKHB1 for Pleckstrin-Homology-domain-containingprotein-family-B-member-1), transcription/translation (eukaryotic-translation-elongation-factor-1-a1) processes and cell adhesion (SPOCK1 for SPARC/Osteonectin-CWCV-kazal-like-domains-proteoglycan). The expression of these genes was confirmed by real-time quantitative RT-PCR and immunohistochemistry. This study highlights the crucial role of brain invasion in GBM and identifies specific molecules involved in this process. In addition, it offers a restricted list of markers that accurately distinguish PA from GBM.

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Testican-1: A Differentially Expressed Proteoglycan with Protease Inhibiting Activities

Cited by 47 publications

References 37 publications

Testican-1 is dispensable for mouse development

Testican-1 is dispensable for mouse development

Plakophilin 1-deficient cells upregulate SPOCK1: implications for prostate cancer progression

Identification of genes differentially expressed in glioblastoma versus pilocytic astrocytoma using Suppression Subtractive Hybridization

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