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Endogenous expression of the R-RAS2 GTPase carrying the Q72L hotspot mutation is relevant for the tumorigenic phenotype of cancer cells

ABSTRACT: The R-RAS2 GTPase has been considered quite similar to classical RAS proteins at the regulatory, signaling, and functional level. The interest in this GTPase has been reinvigorated upon the recent discovery that a long-tail hotspot RRAS2 mutation found in human tumors (Gln72 to Leu) can act as a potent oncogenic driver. Here, we report that the Q72L mutation and other gain-of-function mutations of RRAS2 play roles in tumor initiation and maintenance. Such roles are unlikely to be redundant to those normally executed by classical RAS proteins.

ORGANISM(S): Homo sapiens

PROVIDER: GSE201472 | GEO | 2022/12/03

REPOSITORIES: GEO

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A hotspot mutation targeting the R-RAS2 GTPase acts as a potent oncogenic driver in a wide spectrum of tumors

Project description:A missense change in RRAS2 (Gln72-to-Leu), analogous to the Gln61-to-Leu mutation of RAS oncoproteins, has been identified as a hotspot mutation in cancer and Noonan syndrome. However, the relevance of this mutation for in vivo tumorigenesis remains unknown. Here, we show that R-RAS2(Q72L) is required for optimal tumorigenic activity of human cancer cells.

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R-Ras2 is required for germinal center formation to aid B cells during energetically demanding processes

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Endogenous expression of the R-RAS2 GTPase carrying the Q72L hotspot mutation is relevant for the tumorigenic phenotype of cancer cells

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Expression data from human breast cancer cells MDA-MB-231-Luc knockdown for RRAS2 expression.

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Expression data from human breast cancer cells MDA-MB-231-Luc knockdown for RRAS2 expression.

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