The Kindlin2-p53-SerpinB2 signaling axis is required for cellular senescence in breast cancer.

ABSTRACT: In cancer, cellular senescence is a complex process that leads to inhibition of proliferation of cells that may develop a neoplastic phenotype. A plethora of signaling pathways, when dysregulated, have been shown to elicit a senescence response. Two well-known tumor suppressor pathways, controlled by the p53 and retinoblastoma proteins, have been implicated in maintaining the cellular senescence phenotype. Kindlin-2, a member of an actin cytoskeleton organizing and integrin activator proteins, has been shown to play a key role in the regulation of several hallmarks of several cancers, including breast cancer (BC). The molecular mechanisms whereby Kindlin-2 regulates cellular senescence in BC tumors remains largely unknown. Here we show that Kindlin-2 regulates cellular senescence in part t

SUBMITTER: Sossey-Alaoui K 

PROVIDER: S-EPMC6629707 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature