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FGFR inhibitors, particularly BGJ398, are therapeutic options for cholangiocarcinoma patients harboring FGFR2-CCDC6 fusions.
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Our findings nevertheless suggest that CCDC6-RET fusions identified by multiplex testing are potential targets for nintedanib therapy.
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we propose that the amount of CCDC6 protein in primary tumors, as reported in lung, may depend on the impairment of the CCDC6 turnover due to altered protein-protein interaction and post-translational modifications
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Results show that RNA-binding protein EWS binds and regulates CCDC6 expression at RNA and protein levels.
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CCDC6 levels provide valuable insight for OS.
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the loss of CCDC6 could aid the spermatogonial cells to be part of a pro-survival pathway that helps to evade the toxic effects of endogenous oxidants and contributes to testicular neoplastic growth.
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Expression of the CCDC6-RET fusion gene in LC-2/ad cells was demonstrated by the mRNA and protein levels, and the genomic break-point was confirmed by genomic DNA sequencing.
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CCDC6 is associated with cAMP signaling by fine regulating CREB1 transcriptional activity in normal and transformed thyroid cells.
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CCDC6-RET fusion is associated with lung adenocarcinoma.
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It was shown that FBXW7 interacts with and targets CCDC6 for ubiquitin-mediated proteasomal degradation. FBXW7-mediated CCDC6 degradation was impaired in response to DNA damage.
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Following genotoxic stress, loss or inactivation of CCDC6 in cancers that carry the CCDC6 fusion, accelerates the dephosphorylation of pH2AX S139, resulting in defective G2 arrest and premature mitotic entry.
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CCDC6 plays a key role in cell cycle control.
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we discovered previously unidentified kinase fusions that may be promising for molecular-targeted therapy, kinesin family member 5B (KIF5B)-ret proto-oncogene (RET) and coiled-coil domain containing 6 (CCDC6)-RET, in 14 adenocarcinomas
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down-regulation of 14-3-3sigma in the absence of CCDC6 demonstrated their direct association and supports the notion that CCDC6 contributes to cancer development, possibly through malignant pathways involving 14-3-3sigma
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repression of CREB1 activity by CCDC6 has a critical function in the development of human thyroid papillary carcinomas carrying RET/PTC1 activation.
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H4(D10S170) is involved in the cellular response to ataxia telangectasia mutated (ATM) kinase; impairment of H4(D10S170) gene function might have a role in thyroid carcinogenesis.
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frequency of the occurrence of BRAF mutation and/or RET/PTC in H4-PTEN positive tumors was extremely high (75%) in papillary thyroid carcinoma
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PTC1 and PTC3 are highly oncogenic proteins when overexpressed, but result in indolent disease compared with RET-related MTCs due to their relatively low expression from the NCOA4 and CCDC6 promoters in vivo.
