Prognostic impact of ARHGAP43(SH3BP1) in acute myeloid leukemia

Yang, Li; Xu, Qiang; Li, Junnan

doi:10.1016/j.jfma.2024.04.002

Cited by 1 publication

(1 citation statement)

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“…ARHGAP43 is overexpressed in patients with acute myeloid leukaemia, and the downregulation of ARHGAP43 expression inhibits the proliferation of AML cells. 15 Additionally, the ARHGAP‐RhoA signalling pathway causes homotypic adhesion‐triggered cell death in metastatic diffuse‐type gastric cancer. 16 However, the role of ARHGAPs as a pro‐carcinogenic factor in glioma has not been studied, especially in the immune microenvironment, and the mechanism of action has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

A novel ARHGAP family gene signature for survival prediction in glioma patients

Huang,

Wang,

Zhang

et al. 2024

J Cellular Molecular Medi

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ARHGAP family genes are often used as glioma oncogenic factors, and their mechanism of action remains unexplained. Our research entailed a thorough examination of the immune microenvironment and enrichment pathways across various glioma subtypes. A distinctive 6‐gene signature was developed employing the CGGA cohort, leading to insights into the disparities in clinical characteristics, mutation patterns, and immune cell infiltration among distinct risk categories. Additionally, a unique nomogram was established, grounded on ARHGAPs, with DCA curves illustrating the model's prospective clinical utility in guiding therapeutic strategies. Emphasizing the role of ARHGAP30, integral to our model, its impact on glioma severity and the credibility of our risk assessment model were substantiated through RT‐qPCR, Western blot analysis, and cellular functional assays. We identified 6 ARHGAP family genes associated with glioma prognosis. Analysis using the Kaplan–Meier method indicated a correlation between elevated risk levels and adverse outcomes in glioma patients. The risk score, linked with tumour staging and IDH mutation status, emerged as an independent factor predicting prognosis. Patients in the high‐risk category exhibited increased immune cell infiltration, enhanced tumour mutational burden, more pronounced expression of immune checkpoint genes, and a better response to ICB therapy. A nomogram, integrating the risk score with the pathological features of glioma patients, was developed. DCA analysis and cellular studies confirmed the model's potential to improve clinical treatment outcomes for patients. A novel ARHGAP family gene signature reveals the prognosis of glioma.

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Section: Introductionmentioning

confidence: 99%