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Caveolin-1 regulates context-dependent signaling and survival in Ewing Sarcoma. | LitMetric

AI Article Synopsis

  • Cellular plasticity is crucial in cancer, but its mechanisms are largely unclear; this study identifies Caveolin-1 as an important regulator of survival signaling specifically in Ewing sarcoma (EwS).
  • Analysis shows a unique subgroup of EwS cells marked by high CD99 and Caveolin-1 expression, exhibiting differences in appearance, gene expression, and survival when compared to low CD99 cells.
  • The research indicates that high Caveolin-1 levels in these cells create a specific signaling network that enhances survival through localized PI3K/AKT activity, suggesting a transition in EwS cell states influenced by Caveolin-1.

Article Abstract

Cellular plasticity is a hallmark function of cancer, but many of the underlying mechanisms are not well understood. We uncover Caveolin-1, a scaffolding protein that modulates plasma membrane domain organization, as a context-specific regulator of survival signaling in Ewing sarcoma (EwS). Single cell analysis reveals a distinct subpopulation of EwS cells, which highly express the cell surface marker CD99 as well as Caveolin-1. CD99 High cells isolated through flow cytometry differ from CD99 Low cells in morphology, gene expression, and survival capabilities in vivo. Our work demonstrates that elevated Caveolin-1 expression in these cells plays a key role in the regulation of PI3K/AKT survival signaling, through subcellular organization of PI3K activity at the cell surface. We thus propose a model where the CD99 High state develops a Cav-1 controlled signaling network to regulate cell survival that is distinct from the AKT-agnostic survival of CD99 Low cells. Overall, this work identifies a state transition of EwS cells and uncovers Caveolin-1 as a driver of survival signaling in a context-dependent manner.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661136PMC
http://dx.doi.org/10.1101/2024.09.23.614468DOI Listing

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