{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jin JY"],"funding":["NIAMS NIH HHS"],"pagination":["1149-58"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3108157"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["131(5)"],"pubmed_abstract":["Deregulation of the activator protein 1 (AP1) family gene regulators has been implicated in a wide range of diseases, including cancer. In this study we report that c-Jun was activated in human squamous cell carcinoma (SCC) and coexpression of c-Jun with oncogenic Ras was sufficient to transform primary human epidermal cells into malignancy in a regenerated human skin grafting model. In contrast, JunB was not induced in a majority of human SCC cells. Moreover, exogenous expression of JunB inhibited tumorigenesis driven by Ras or spontaneous human SCC cells. Conversely, the dominant-negative JunB mutant (DNJunB) promoted tumorigenesis, which is in contrast to the tumor-suppressor function of the corresponding c-Jun mutant. At the cellular level, JunB induced epidermal cell senescence and sl"],"journal":["The Journal of investigative dermatology"],"pubmed_title":["c-Jun promotes whereas JunB inhibits epidermal neoplasia."],"pmcid":["PMC3108157"],"funding_grant_id":["K01 AR051470-05","R01 AR057746-01A1","K01 AR051470-04","R01 AR057746","R01AR57746","K01 AR051470","K01AR051470"],"pubmed_authors":["Jin JY","Ke H","Zhang JY","Hall RP"],"additional_accession":[]},"is_claimable":false,"name":"c-Jun promotes whereas JunB inhibits epidermal neoplasia.","description":"Deregulation of the activator protein 1 (AP1) family gene regulators has been implicated in a wide range of diseases, including cancer. In this study we report that c-Jun was activated in human squamous cell carcinoma (SCC) and coexpression of c-Jun with oncogenic Ras was sufficient to transform primary human epidermal cells into malignancy in a regenerated human skin grafting model. In contrast, JunB was not induced in a majority of human SCC cells. Moreover, exogenous expression of JunB inhibited tumorigenesis driven by Ras or spontaneous human SCC cells. Conversely, the dominant-negative JunB mutant (DNJunB) promoted tumorigenesis, which is in contrast to the tumor-suppressor function of the corresponding c-Jun mutant. At the cellular level, JunB induced epidermal cell senescence and sl","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 May","modification":"2025-04-04T07:38:13.351Z","creation":"2019-03-27T00:42:17Z"},"accession":"S-EPMC3108157","cross_references":{"pubmed":["21289643"],"doi":["10.1038/jid.2011.1"]}}