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http://purl.uniprot.org/citations/21103065http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21103065http://www.w3.org/2000/01/rdf-schema#comment"

Background

We determined recently that dentin sialophosphoprotein (DSPP), a member of the SIBLING (Small integrin-binding ligand N-linked glycoproteins) family of phosphoglycoproteins, is highly upregulated in human oral squamous cell carcinomas (OSCCs) where upregulation is associated with tumor aggressiveness. To investigate the effects of DSPP-silencing on the tumorigenic profiles of the oral cancer cell line, OSC2, short-hairpin RNA (shRNA) interference was employed to silence DSPP in OSC2 cells.

Methodology/principal findings

Multiple regions of DSPP transcript were targeted for shRNA interference using hDSP-shRNA lentiviral particles designed to silence DSPP gene expression. Control shRNA plasmid encoding a scrambled sequence incapable of degrading any known cellular mRNA was used for negative control. Following puromycin selection of stable lines of DSSP-silenced OSC2 cells, phenotypic hallmarks of oral carcinogenesis were assayed by western blot and RT-PCR analyses, MTT (cell-viability), colony-formation, modified Boyden-Chamber (migration and invasion), and flow cytometry (cell-cycle and apoptosis) analyses. DSPP-silenced OSC2 cells showed altered cell morphology, reduced viability, decreased colony-formation ability, decreased migration and invasion, G0/G1 cell-cycle arrest, and increased tumor cell sensitivity to cisplatin-induced apoptosis. Furthermore, MMP-2, MMP-3, MMP-9, VEGF, Ki-67, p53, and EGFR were down-regulated. There was a direct correlation between the degree of DSPP-silencing and MMP suppression, as indicated by least squares regression: MMP-2 {(y = 0.850x, p<0.001) (y = 1.156x, p<0.001)}, MMP-3 {(y = 0.994x, p<0.001) (y = 1.324x, p = 0.004)}, and MMP-9 {(y = 1.248x, p = 0.005, y = 0.809, p = 0.013)}.

Conclusions/significance

DSPP-silencing in OSC2 cell decreased salient hallmarks of oral tumorigenesis and provides the first functional evidence of a potential key role for DSPP in oral cancer biology. The down-regulation of MMP-2, MMP-3, MMP-9, p53 and VEGF in DSPP-silenced OSC2 cells provides a significant functional/molecular framework for deciphering the mechanisms of DSPP activities in oral cancer biology."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0013974"xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Lewis J."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Hsu S."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Joshi R."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Ogbureke K.U."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Looney S."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Tawfik A."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"Edeh N."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/author"McCloud V."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/pages"e13974"xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/title"Dentin sialophosphoprotein (DSPP) gene-silencing inhibits key tumorigenic activities in human oral cancer cell line, OSC2."xsd:string
http://purl.uniprot.org/citations/21103065http://purl.uniprot.org/core/volume"5"xsd:string
http://purl.uniprot.org/citations/21103065http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21103065
http://purl.uniprot.org/citations/21103065http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21103065
http://purl.uniprot.org/uniprot/#_A0A0U3J4I2-mappedCitation-21103065http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21103065
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