AI Article Synopsis

  • CCDC6 is often rearranged in papillary thyroid carcinomas, aiding in the creation of the RET/PTC1 oncogene and showing high susceptibility to chromosomal changes.
  • The study aimed to identify proteins that are affected by the silencing of CCDC6, which may link its deregulation to cancer.
  • Down-regulation of the protein 14-3-3σ was found when CCDC6 was silenced, indicating a direct association that suggests CCDC6 plays a role in cancer development through pathways involving 14-3-3σ.

Article Abstract

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.

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