ArticleCancer biology & therapy2026
ARHGAP40 suppresses clear cell renal cell carcinoma progression and is associated with altered glutamine-related metabolism and redox balance.
Article in Cancer biology & therapy, 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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Abstract
objectiveClear cell renal cell carcinoma (ccRCC) is characterized by marked molecular and metabolic heterogeneity. This study investigated the functional role of ARHGAP40 in ccRCC and examined signaling and metabolic changes associated with ARHGAP40 expression.
methodsTCGA-KIRC and DiseaseMeth datasets were used to analyze ARHGAP40 expression and promoter methylation. Gain- and loss-of-function experiments evaluated malignant phenotypes
resultsARHGAP40 was downregulated in ccRCC and was associated with increased promoter methylation. ARHGAP40 overexpression suppressed cell proliferation, migration, invasion, EMT, and xenograft growth, while promoting apoptosis and G1-phase arrest; ARHGAP40 knockdown produced the opposite effects. Mechanistically, ARHGAP40 was associated with RhoA, and its overexpression was accompanied by reduced RhoA activity and PI3K/AKT phosphorylation. ARHGAP40 overexpression also reduced intracellular glutamine and glutamate levels and net glutamine consumption, decreased the GSH/GSSG ratio, and increased ROS levels. SC79 and RhoA-Q63L partially reversed the biological and redox effects induced by ARHGAP40 overexpression, whereas NAC reversed the redox changes.
conclusionARHGAP40 acts as a tumor suppressor in ccRCC. Our findings support a functional link between ARHGAP40, RhoA-PI3K/AKT signaling, glutamine-related metabolism, and cellular redox balance.
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