ArticleCancer biology & therapy2025
GNAQ inhibits tumorigenesis via the ARHGEF25-mediated RHOA pathway in NK/T-cell lymphoma.
Article in Cancer biology & therapy, 2025. 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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Abstract
backgroundNatural killer/T-cell lymphoma (NKTCL) presents highly aggressive clinical behaviour, and the outcomes for relapsed and refractory patients are still poor. Our previous study identified somatic mutations in GNAQ in 8.7% of cases through whole-exome sequencing, revealing the T96S mutation in the Gαq protein. MATERIALS: The proliferation, gemcitabine sensitivity and apoptosis of NKTCL cells were assessed by CCK-8 assays and flow cytometry. The downstream pathways of GNAQ were explored by mRNA sequencing, Western blotting and co‑immunoprecipitation. Additionally, we investigated the role of GNAQ in the activation of the RHOA pathway in NKTCL.
resultsWe found that GNAQ significantly inhibited the aggressive function of NKTCL, whereas the T96S mutation abolished the ability of wild-type GNAQ to trigger cell apoptosis. Further investigation revealed that GNAQ modulated NKTCL cell functions through the activation of the RHOA pathway, which is regulated by the GNAQ-ARHGEF25 complex. Clinically, high expression of RHOA was associated with improved overall survival (HR = 0.317, 95% CI: 0.126-0.800,
conclusionIn summary, RHOA is a critical downstream effector of GNAQ in NKTCL. GNAQ promotes RHOA activation through ARHGEF25, which in turn regulates cellular functions by modulating cell proliferation and apoptosis, thereby influencing the progression of NKTCL.
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