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Annexin A5 as a New Potential Biomarker for Cisplatin-Induced Toxicity in Human Kidney Epithelial Cells
Article en En | WPRIM | ID: wpr-202365
Biblioteca responsable: WPRO
ABSTRACT
Cisplatin is a member of platinum-containing anti-cancer drugs that causes cross-linking of DNA and ultimately cancer cell apoptosis. The therapeutic function of cisplatin on various types of cancers has been widely reported but the side effects have been discovered together and nephrotoxicity has been regarded as major side effect of cisplatin. To select candidates for new sensitive nephrotoxicity biomarker, we performed proteomic analysis using 2-DE/MALDI-TOF-MS followed by cisplatin treatment in human kidney cell line, HK-2 cells, and compared the results to the gene profi le from microarray composed of genes changed in expression by cisplatin from formerly reported article. Annexin A5 has been selected to be the most potential candidate and it has been identifi ed using Western blot, RT-PCR and cell viability assay whether annexin A5 is available to be a sensitive nephrotoxic biomarker. Treatment with cisplatin on HK-2 cells caused the increase of annexin A5 expression in protein and mRNA levels. Overexpression of annexin A5 blocked HK-2 cell proliferation, indicating correlation between annexin A5 and renal cell toxicity. Taken together, these results suggest the possibility of annexin A5 as a new biomarker for cisplatin-mediated nephrotoxicity.
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Texto completo: 1 Índice: WPRIM Asunto principal: ADN / ARN Mensajero / Línea Celular / Supervivencia Celular / Western Blotting / Cisplatino / Apoptosis / Anexina A5 / Proliferación Celular / Células Epiteliales Límite: Humans Idioma: En Revista: Biomolecules & Therapeutics Año: 2013 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Asunto principal: ADN / ARN Mensajero / Línea Celular / Supervivencia Celular / Western Blotting / Cisplatino / Apoptosis / Anexina A5 / Proliferación Celular / Células Epiteliales Límite: Humans Idioma: En Revista: Biomolecules & Therapeutics Año: 2013 Tipo del documento: Article