ArticleFrontiers in medicine2026
Downregulation of PRPS2 inhibits tumor growth of non-small cell lung cancer by suppressing PI3K/AKT signaling.
Article in Frontiers in medicine, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Introduction: This study aims to investigate the role of phosphoribosyl pyrophosphate synthetases 2 (PRPS2) in non-small cell lung cancer (NSCLC) and its underlying molecular mechanisms. Methods: The expression patterns of PRPS2 were analyzed in databases, and its expression levels were validated by RT-qPCR. Stable cell lines with PRPS2 knockdown and overexpression were established. In addition, MTT and colony formation assays were conducted to determine cell proliferation. Western blotting and RT-qPCR assays were conducted to evaluate changes in PI3K/AKT signaling and cell cycle proteins. Furthermore, a cell line-derived xenograft animal model was utilized to confirm the roles of PRPS2 Results: An elevation of PRPS2 was observed in NSCLC samples, and its overexpression promoted NSCLC cell proliferation, while PRPS2 knockdown inhibited cell proliferation. Additionally, PRPS2 overexpression promoted the PI3K/AKT signaling pathway in NSCLC cells. Moreover, PRPS2 regulated the expression of downstream genes in the PI3K/AKT pathway. Consistently, PRPS2 knockdown suppressed NSCLC tumor growth Conclusion: PRPS2 promotes tumor growth of NSCLC through the regulation of the activation of the PI3K/AKT signaling pathway. Targeting PRPS2 may be a promising strategy for the therapy of NSCLC in the future.
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