<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hishida T</submitter><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>786031</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8931341</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10</volume><pubmed_abstract>It is widely believed that cellular senescence plays a critical role in both aging and cancer, and that senescence is a fundamental, permanent growth arrest that somatic cells cannot avoid. Here we show that Myc plays an important role in self-renewal of esophageal epithelial cells, contributing to their resistance to cellular senescence. Myc is homogeneously expressed in basal cells of the esophageal epithelium and Myc positively regulates their self-renewal by maintaining their undifferentiated state. Indeed, Myc knockout induced a loss of the undifferentiated state of esophageal epithelial cells resulting in cellular senescence while forced MYC expression promoted oncogenic cell proliferation. A superoxide scavenger counteracted Myc knockout-induced senescence, therefore suggesting that</pubmed_abstract><journal>Frontiers in cell and developmental biology</journal><pubmed_title>Myc Supports Self-Renewal of Basal Cells in the Esophageal Epithelium.</pubmed_title><pmcid>PMC8931341</pmcid><funding_grant_id>R01 NS106878</funding_grant_id><funding_grant_id>R01 GM116919</funding_grant_id><pubmed_authors>Sahu SK</pubmed_authors><pubmed_authors>O'Keefe DD</pubmed_authors><pubmed_authors>Hishida-Nozaki Y</pubmed_authors><pubmed_authors>Nunez Delicado E</pubmed_authors><pubmed_authors>Kato R</pubmed_authors><pubmed_authors>Izpisua Belmonte JC</pubmed_authors><pubmed_authors>Hatanaka F</pubmed_authors><pubmed_authors>Yoshida K</pubmed_authors><pubmed_authors>Rodriguez Esteban C</pubmed_authors><pubmed_authors>Takahashi Y</pubmed_authors><pubmed_authors>Knoepfler PS</pubmed_authors><pubmed_authors>Nakagawa H</pubmed_authors><pubmed_authors>Takemoto Y</pubmed_authors><pubmed_authors>Castells A</pubmed_authors><pubmed_authors>Hishida T</pubmed_authors><pubmed_authors>Vazquez-Ferrer E</pubmed_authors><pubmed_authors>Prieto J</pubmed_authors><pubmed_authors>Reddy P</pubmed_authors><pubmed_authors>Campistol JM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Myc Supports Self-Renewal of Basal Cells in the Esophageal Epithelium.</name><description>It is widely believed that cellular senescence plays a critical role in both aging and cancer, and that senescence is a fundamental, permanent growth arrest that somatic cells cannot avoid. Here we show that Myc plays an important role in self-renewal of esophageal epithelial cells, contributing to their resistance to cellular senescence. Myc is homogeneously expressed in basal cells of the esophageal epithelium and Myc positively regulates their self-renewal by maintaining their undifferentiated state. Indeed, Myc knockout induced a loss of the undifferentiated state of esophageal epithelial cells resulting in cellular senescence while forced MYC expression promoted oncogenic cell proliferation. A superoxide scavenger counteracted Myc knockout-induced senescence, therefore suggesting that</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T14:50:07.481Z</modification><creation>2025-04-04T14:50:07.481Z</creation></dates><accession>S-EPMC8931341</accession><cross_references><pubmed>35309931</pubmed><doi>10.3389/fcell.2022.786031</doi></cross_references></HashMap>