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Phosphoribosyl pyrophosphate synthetases 2 ( PRPS2 ) is reported as an oncogene in various cancers. However, the role of  PRPS2  in cisplatin (DDP) resistance of non-small cell lung cancer (NSCLC) remains unclear. The present study aimed to explore the effect of  PRPS2  in DDP resistance of NSCLC. mRNA expression levels of genes were detected by RT-PCR. Enzyme-linked immunosorbent assay (ELISA) and Western blot were used to detect protein expression levels. Cell viability was determined by the MTT assay and colony formation assay. Cell apoptosis was detected using nucleosome ELISA assay and caspase-3 activity assay.  PRPS2  silencing was achieved using siRNA transfection. Exosomes of cultured cells were isolated through ultracentrifugation. Elevated  PRPS2  was correlated with DDP resistance and poor prognosis in NSCLC patients.  PRPS2  silencing enhanced sensitivity of DDP-resistant cells to DDP treatment. NSCLC cell-derived exosome induced M2 macrophage polarization.  PRPS2  was enriched in the exosomes of NSCLC cells. Exosomal PRPS2 mediated M2 macrophage polarization to promote DDP resistance of NSCLC cells. In conclusion,  PRPS2  potentiates resistance to DDP by promoting exosome-mediated macrophage M2 polarization in NSCLC.

PRPS2 Enhances Resistance to Cisplatin via Facilitating Exosomes-mediated Macrophage M2 Polarization in Non-small Cell Lung Cancer