Silencing of CCDC6 Reduces the Expression of 14-3-3σ in Colorectal Carcinoma Cells

Coiled-coil domain containing 6 (CCDC6) is frequently rearranged in papillary thyroid carcinomas participating in the formation of RET/PTC1 oncogene. Other rearrangements involving CCDC6 have also been identified demonstrating its high susceptibility to chromosomal recombination. Malignancies bearin...

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Bibliographic Details
Published in:Anticancer research 2012-03, Vol.32 (3), p.907-913
Main Authors: THANASOPOULOU, Angeliki, XANTHOPOULOU, Alexandra G, ANAGNOSTOPOULOS, Athanasios K, KONSTANTAKOU, Eumorphia G, MARGARITIS, Lukas H, PAPASSIDERI, Isidora S, STRAVOPODIS, Dimitrios J, TSANGARIS, George T, ANASTASIADOU, Ema
Format: Article
Language:English
Subjects:
14-3-3 Proteins - metabolism
Base Sequence
Biological and medical sciences
Biomarkers, Tumor - metabolism
Cell Line, Tumor
Colorectal Neoplasms - metabolism
Colorectal Neoplasms - pathology
Cytoskeletal Proteins - genetics
DNA Primers
Down-Regulation
Electrophoresis, Gel, Two-Dimensional
Exonucleases - metabolism
Exoribonucleases
Gastroenterology. Liver. Pancreas. Abdomen
Gene Knockdown Techniques
Gene Silencing
Humans
Medical sciences
Proteomics
Reverse Transcriptase Polymerase Chain Reaction
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumors
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Summary:Coiled-coil domain containing 6 (CCDC6) is frequently rearranged in papillary thyroid carcinomas participating in the formation of RET/PTC1 oncogene. Other rearrangements involving CCDC6 have also been identified demonstrating its high susceptibility to chromosomal recombination. Malignancies bearing CCDC6 fusion genes are developed in a background where CCDC6 is either lost or deregulated. Our aim was to identify interacting proteins which are affected by the silencing of CCDC6 expression and could possibly link CCDC6 deregulation to cancer causality. Therefore, a proteomic approach was adopted using a human cancer cell-line (HCT116) where CCDC6 expression was silenced by lentiviral shRNA constructs. 14-3-3σ down-regulation in the absence of CCDC6 was revealed and verified by western blot analysis and confocal microscopy. Only the levels and not the topology of CCDC6 were altered. The down-regulation of 14-3-3σ in the absence of CCDC6 demonstrated their direct association and supports the notion that CCDC6 contributes to cancer development, possibly through malignant pathways involving 14-3-3σ.
ISSN:0250-7005
1791-7530