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Research Article: Downregulation of PRPS2 inhibits tumor growth of non-small cell lung cancer by suppressing PI3K/AKT signaling

Date Published: 2026-05-12

Abstract:
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. 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 in vivo . 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 in vivo . In addition, PRPS2 was found downregulated by the natural compound pristimerin in NSCLC cells. 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.

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.

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