The proteomic 2D-DIGE approach reveals the protein voltage-dependent anion channel 2 as a potential therapeutic target in epithelial thyroid tumours. (15th March 2015)

• Record Type: Journal Article
• Authors: Mato, Eugenia; Barceló-Batllori, Sílvia; Orera, Irene; Selva, Laia; Corra, Martina; González, Cintia; Bell, Olga; Lerma, Enrique; Moral, Antonio; Pérez, José Ignacio; de Leiva, Alberto
• Is Part Of: Molecular and cellular endocrinology. Volume 404(2015)
• Page Start: 37
• Page End: 45
• Publication Date: 2015-03-15
• Subjects: Voltage-dependent anion channel 2 -- Epithelial thyroid tumours -- Therapeutic target; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2015.01.021
• Languages: English
• ISSNs: 0303-7207

Abstract

Highlights: We propose the mitochondrial VACD2 protein as a novel gene for developing therapeutic strategies. The proteomic 2D-DIGE system is a useful tool to identify new candidate genes. The 2D-DIGE analysis is a useful tool to compare differentially expressed proteins in epithelial thyroid carcinoma. Abstract: We investigated the role of VDAC2 in human epithelial thyroid tumours using proteomic 2D-DIGE analysis and qRT-PCR. We found a significant up-regulation of VDAC2 in thyroid tumours and in thyroid tumour cell lines (TPC-1 and CAL-62). We did not detect overexpression of VDAC2 in a normal thyroid cell line (Nthy-ori 3-1). Silico analysis revealed that two proteins, BAK1 and BAX, had a strong relationship with VDAC2. BAK1 gene expression showed down-regulation in thyroid tumours (follicular and papillary tumours) and in TPC-1 and CAL-62 cell lines. Transient knockdown of VDAC2 in TPC-1 and CAL-62 promoted upregulation of the BAK1 gene and protein expression, and increased susceptibility to sorafenib treatment. Overexpression of the BAK1 gene in CAL-62 showed lower sorafenib sensitivity than VDAC2 knockdown cells. We propose the VDAC2 gene as a novel therapeutic target in these tumours.