{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cheung BB"],"funding":["Cancer Council NSW","Cancer Research UK","National Health and Medical Research Council Australia","Cancer Institute NSW","Re-use of this article is permitted in accordance with the Terms and Conditions set out at  [http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms]"],"pagination":["451-62"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3504077"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["226(3)"],"pubmed_abstract":["Retinoid therapy is used for chemo-prevention in immuno-suppressed patients at high risk of developing skin cancer. The retinoid signalling molecule, tripartite motif protein 16 (TRIM16), is a regulator of keratinocyte differentiation and a tumour suppressor in retinoid-sensitive neuroblastoma. We sought to determine the role of TRIM16 in skin squamous cell carcinoma (SCC) pathogenesis. We have shown that TRIM16 expression was markedly reduced during the histological progression from normal skin to actinic keratosis and SCC. SCC cell lines exhibited lower cytoplasmic and nuclear TRIM16 expression compared with primary human keratinocyte (PHK) cells due to reduced TRIM16 protein stability. Overexpressed TRIM16 translocated to the nucleus, inducing growth arrest and cell differentiation. In "],"journal":["The Journal of pathology"],"pubmed_title":["The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro."],"pmcid":["PMC3504077"],"funding_grant_id":["13044"],"pubmed_authors":["Proby C","D'andreti C","Wilmott JS","Bell JL","Malyukova A","Cunningham AM","Kim P","Koach J","Cooper CL","Cheung BB","Kavallaris M","Leigh I","Sutton S","Norris M","Marshall GM","Haber M","Tan O","Sekyere E","Scolyer RA","Halliday GM"],"additional_accession":[]},"is_claimable":false,"name":"The retinoid signalling molecule, TRIM16, is repressed during squamous cell carcinoma skin carcinogenesis in vivo and reduces skin cancer cell migration in vitro.","description":"Retinoid therapy is used for chemo-prevention in immuno-suppressed patients at high risk of developing skin cancer. The retinoid signalling molecule, tripartite motif protein 16 (TRIM16), is a regulator of keratinocyte differentiation and a tumour suppressor in retinoid-sensitive neuroblastoma. We sought to determine the role of TRIM16 in skin squamous cell carcinoma (SCC) pathogenesis. We have shown that TRIM16 expression was markedly reduced during the histological progression from normal skin to actinic keratosis and SCC. SCC cell lines exhibited lower cytoplasmic and nuclear TRIM16 expression compared with primary human keratinocyte (PHK) cells due to reduced TRIM16 protein stability. Overexpressed TRIM16 translocated to the nucleus, inducing growth arrest and cell differentiation. In ","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Feb","modification":"2025-07-06T03:05:43.769Z","creation":"2025-07-06T03:05:43.769Z"},"accession":"S-EPMC3504077","cross_references":{"pubmed":["22009481"],"doi":["10.1002/path.2986"]}}