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http://purl.uniprot.org/citations/24362251http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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CABYR is a calcium-binding tyrosine phosphorylation-regulated protein that was identified as a novel cancer testis antigen in lung cancer in our previous study. However, the role of CABYR as a driver of disease progression or as a chemosensitizer is poorly understood. This study sought to investigate the relationship between the expression levels of CABYR-a/b, which are the two predominant isoforms of the five isoform proteins encoded by CABYR, and chemosensitivity in non-small cell lung cancer cells. We found that the short hairpin RNA-mediated knockdown of CABYR-a/b significantly inhibited the proliferation of NCI-H460 and A549 cells and resulted in the attenuation of Akt phosphorylation, which is constitutively active in lung cancer cells. The silencing of CABYR-a/b expression notably impacted the downstream components of the Akt pathways: decreasing the phospho-GSK-3β (Ser9) levels and increasing the expression of the p53 and p27 proteins. Furthermore, CABYR-a/b knockdown led to a significant increase in chemosensitivity in response to chemotherapeutic drugs and drug-induced apoptosis, both in vitro and in vivo. Conversely, the transient transfection of CABYR-a/b-depleted cells with constitutively active Akt partially restored the resistance to cisplatin and paclitaxel and significantly decreased the activation of GSK-3β and cleaved PARP. Taken together, our results suggest that the inhibition of CABYR-a/b is a novel method to improve the apoptotic response and chemosensitivity in lung cancer and that this cancer testis antigen is an attractive target for lung cancer drug development.

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Suppression of CABYR-a/b expression increases chemosensitivity of lung cancer cells by inhibiting Akt activity."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.org/dc/terms/identifier"doi:10.1158/1541-7786.mcr-13-0391"xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Qian Z."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Xiao X."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Wang R."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Xiao Q."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"He D."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/author"Li M.'"xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/name"Mol Cancer Res"xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/pages"335-347"xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/title"Knockdown of CABYR-a/b increases chemosensitivity of human non-small cell lung cancer cells through inactivation of Akt."xsd:string
http://purl.uniprot.org/citations/24362251http://purl.uniprot.org/core/volume"12"xsd:string
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