Cellular Senescence Promotes Skin Carcinogenesis through p38MAPK and p44/42MAPK Signaling.

ABSTRACT: Cellular senescence entails an irreversible growth arrest that evolved in part to prevent cancer. Paradoxically, senescent cells secrete proinflammatory and growth-stimulatory molecules, termed the senescence-associated secretory phenotype (SASP), which is correlated with cancer cell proliferation in culture and xenograft models. However, at what tumor stage and how senescence and the SASP act on endogenous tumor growth in vivo is unknown. To understand the role of senescence in cancer etiology, we subjected p16-3MR transgenic mice, which permit the identification and selective elimination of senescent cells in vivo, to the well-established two-step protocol of squamous cell skin carcinoma, in which tumorigenesis is initiated by a carcinogen 7,12-dimethylbenz[α]anthracene, an

SUBMITTER: Alimirah F 

PROVIDER: S-EPMC7484313 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature