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http://purl.uniprot.org/citations/23026567http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23026567http://www.w3.org/2000/01/rdf-schema#comment"

Objective

There are currently no targeted therapies against lung tumors with oncogenic K-ras mutations that are found in 25% to -40% of lung cancers and are characterized by their resistance to epidermal growth factor receptor inhibitors. The isozyme group IIa secretory phospholipase A(2) (sPLA(2)IIa) is a potential biomarker and regulator of lung cancer cell invasion; however, the relationship between K-ras mutations and sPLA(2)IIa has yet to be investigated. We hypothesize that sPLA(2)IIa modulates lung cancer cell growth in K-ras mutant cells and that sPLA(2)IIa expression in human lung tumors is increased in K-ras mutant tumors.

Methods

Baseline sPLA(2)IIa expression in K-ras mutant lung cancer cell lines (A549, SW1573, H358, H2009) was assessed. Cells were treated with a specific sPLA(2)IIa inhibitor and evaluated for apoptosis and cell viability. Nuclear factor kappa-b (NF-κB) and extracellular signal-regulated kinase 1/2 activity were detected by Western blot. Human tumor samples were evaluated for sPLA(2)IIa mRNA expression by quantitative reverse-transcription polymerase chain reaction.

Results

Cytotoxicity of sPLA(2)IIa inhibition correlates with sPLA(2)IIa expression. Apoptosis in response to sPLA(2) inhibition parallels attenuation in NF-κB activity. In addition, sPLA(2)IIa expression in human tumors correlates with squamous cell pathology and increasing stage of K-ras mutant lung tumors.

Conclusions

Baseline sPLA(2)IIa expression predicts response to sPLA(2)IIa inhibition in some K-ras mutant lung cancer cells. This finding is independent of p53 mutation status. Furthermore, squamous tumors and advanced-stage K-ras mutant tumors express more sPLA(2)IIa. These data support a role for sPLA(2)IIa as a potential global therapeutic target in the treatment of lung cancer."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.org/dc/terms/identifier"doi:10.1016/j.jtcvs.2012.08.064"xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Li H."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Meng X."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Mitchell J.D."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Nemenoff R.A."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Yu J.A."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Weyant M.J."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/author"Fullerton D.A."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/name"J Thorac Cardiovasc Surg"xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/pages"1479-1485"xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/title"Group IIa secretory phospholipase expression correlates with group IIa secretory phospholipase inhibition-mediated cell death in K-ras mutant lung cancer cells."xsd:string
http://purl.uniprot.org/citations/23026567http://purl.uniprot.org/core/volume"144"xsd:string
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