ArticleThe Journal of clinical investigation2026
RhoA WT allele loss unleashes the cancer driver function of RhoA E40Q.
Article in The Journal of clinical investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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15 authors.
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Abstract
Cancer hot spot mutations of unknown function often obscure the functional understanding of the molecular pathways underlying cancer formation and limit the progress of precision medicine. We investigated unresolved driver functions of RHOA in head and neck squamous cell carcinoma. Our investigation reveals that RHOA E40Q is a partial loss-of-function allele that paradoxically promotes tumorigenesis only in the absence of WT RhoA. Therefore, mice expressing RHOA E40Q specifically in keratinocytes lacking WT Rhoa spontaneously developed squamous cell carcinoma and had defective hair shaft formation. Mechanistically, this is related to increased replication stress and genome instability caused by aberrant expression of cell cycle regulators and DNA repair genes, independent of the classical RhoA effectors ROCK and DIAPH. These data establish RHOA E40Q as an unusual, context-dependent oncogenic driver: a seemingly inactive variant that unleashes its tumor-promoting potential only when the WT allele is absent.
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