<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Jin JY</submitter><funding>NIAMS NIH HHS</funding><pagination>1149-58</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3108157</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>131(5)</volume><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</pubmed_abstract><journal>The Journal of investigative dermatology</journal><pubmed_title>c-Jun promotes whereas JunB inhibits epidermal neoplasia.</pubmed_title><pmcid>PMC3108157</pmcid><funding_grant_id>K01 AR051470-05</funding_grant_id><funding_grant_id>R01 AR057746-01A1</funding_grant_id><funding_grant_id>K01 AR051470-04</funding_grant_id><funding_grant_id>R01 AR057746</funding_grant_id><funding_grant_id>R01AR57746</funding_grant_id><funding_grant_id>K01 AR051470</funding_grant_id><funding_grant_id>K01AR051470</funding_grant_id><pubmed_authors>Jin JY</pubmed_authors><pubmed_authors>Ke H</pubmed_authors><pubmed_authors>Zhang JY</pubmed_authors><pubmed_authors>Hall RP</pubmed_authors></additional><is_claimable>false</is_claimable><name>c-Jun promotes whereas JunB inhibits epidermal neoplasia.</name><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</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 May</publication><modification>2025-04-04T07:38:13.351Z</modification><creation>2019-03-27T00:42:17Z</creation></dates><accession>S-EPMC3108157</accession><cross_references><pubmed>21289643</pubmed><doi>10.1038/jid.2011.1</doi></cross_references></HashMap>