Myc Supports Self-Renewal of Basal Cells in the Esophageal Epithelium
2022
Tomoaki Hishida | Tomoaki Hishida | Eric Vazquez-Ferrer | Yuriko Hishida-Nozaki | Yuto Takemoto | Fumiyuki Hatanaka | Kei Yoshida | Javier Prieto | Sanjeeb Kumar Sahu | Yuta Takahashi | Pradeep Reddy | David D. O’Keefe | Concepcion Rodriguez Esteban | Paul S. Knoepfler | Estrella Nuñez Delicado | Antoni Castells | Josep M. Campistol | Ryuji Kato | Hiroshi Nakagawa | Hiroshi Nakagawa | Juan Carlos Izpisua Belmonte
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 a mitochondrial superoxide takes part in inducing senescence. Taken together, these analyses reveal extremely low levels of cellular senescence and senescence-associated phenotypes in the esophageal epithelium, as well as a critical role for Myc in self-renewal of basal cells in this organ. This provides new avenues for studying and understanding the links between stemness and resistance to cellular senescence.
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