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http://purl.uniprot.org/citations/21919028http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21919028http://www.w3.org/2000/01/rdf-schema#comment"

Background

In order for tumors to grow and proliferate, they must avoid recognition by immune cells and subsequent death by apoptosis. Granzyme B (GrB), a protease located in natural killer cells, initiates apoptosis in target cells. Inhibition of GrB by PI-9, its natural inhibitor, can prevent apoptosis. Here we investigate whether PI-9 protects prostate cancer cells from apoptosis.

Methods

The expression of PI-9 was quantified by qPCR in several prostate cancer cell lines, and GrB activity was tested in each cell line. PI-9 was overexpressed in LNCaP cells, which lack endogenous PI-9. Apoptosis was induced by natural killer cells in LNCaP cells that either contained or lacked PI-9, and the percent cell death was quantified. Lastly, PI-9 levels were examined by qPCR and immunohistochemistry in prostate tumor tissue.

Results

Prostate cancer cell lines that expressed PI-9 could inhibit GrB. Overexpression of PI-9 protected LNCaP cells from natural killer cell-mediated apoptosis. Examination of the levels of PI-9 in tissue from prostate tumors showed that PI-9 could be upregulated in low grade tumors and stochastically dysregulated in high grade tumors. Additionally, PI-9 was found consistently in high grade prostatic intraepithelial neoplasia and atrophic lesions.

Conclusions

These results indicate that overexpression of PI-9 can protect prostate cancer cells from apoptosis, and this effect may occur in human prostate tumors. These findings imply that early prostatic inflammation may trigger this increase in PI-9. This suggests that PI-9 upregulation is needed early in tumor progression, before additional protective mechanisms are in place."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.org/dc/terms/identifier"doi:10.1002/pros.21486"xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/author"Craik C.S."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/author"Ray M."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/author"Simko J."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/author"Loeb C.R."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/author"Hostetter D.R."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/name"Prostate"xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/pages"846-855"xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/title"Inhibition of Granzyme B by PI-9 protects prostate cancer cells from apoptosis."xsd:string
http://purl.uniprot.org/citations/21919028http://purl.uniprot.org/core/volume"72"xsd:string
http://purl.uniprot.org/citations/21919028http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21919028
http://purl.uniprot.org/citations/21919028http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21919028
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http://purl.uniprot.org/uniprot/P10144http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/21919028
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