ArticleCancer cell international2026
The mechanistic role of the thromboxane A2 receptor (TBXA2R) in non-small cell lung cancer (NSCLC).
Article in Cancer cell international, 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
Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related death worldwide, underscoring the urgent need for novel therapeutic strategies. The thromboxane A2 receptor (TBXA2R) has gained attention as a pivotal molecule in cancer biology. Our findings reveal a marked overexpression of TBXA2R in NSCLC tissues compared with normal lung tissues, suggesting a possible association with tumorigenesis and disease progression. Furthermore, based on publicly available datasets, higher TBXA2R expression is associated with a reduced survival probability in NSCLC patients. Silencing TBXA2R expression significantly inhibits NSCLC cell proliferation, as evidenced by anchorage-independent growth assays and 3D culture models. RNA sequencing analysis revealed that TBXA2R contributes to NSCLC growth through the activation of the PI3K-AKT and cytokine-cytokine receptor interaction pathways. Notably, TBXA2R knockdown is associated with reduced EGFR expression, accompanied by changes in NF-κB p52 nuclear translocation and its subsequent binding to the EGFR promoter. Additionally, genetic ablation of TBXA2R in mice diminishes both the number and size of urethane-induced lung tumors. Collectively, this study suggests that TBXA2R is involved in NSCLC pathogenesis and may represent a potential therapeutic target. Inhibiting TBXA2R may improve NSCLC treatment outcomes and lessen the impact of this deadly disease.
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