ArticleDiscover oncology2025
CSF2 promotes chemoresistance in colorectal cancer by regulating Notch pathway.
Article in Discover oncology, 2025. 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
backgroundIncreasing evidence suggests that resistance to 5-fluorouracil (5FU) and oxaliplatin (OXP) in colorectal cancer (CRC) is linked to poor prognosis. This study aimed to probe the effect of colony-stimulating factor 2 (CSF2) on the resistance of CRC to 5FU and OXP.
methodsThe expression of CSF2 in CRC and the impact of abnormal CSF2 expression on the prognosis of CRC patients were analyzed using bioinformatics. The half-maximal inhibitory concentrations (IC50) of 5FU and OXP on CRC cells were determined using the CCK-8 assay. Apoptosis in CRC cells was assessed through flow cytometry. mRNA and protein levels were measured using qRT-PCR and western blot, respectively. Gene Set Enrichment Analysis (GSEA) was conduced to investigate the signaling pathways regulated by CSF2 in CRC. The Notch pathway activator Jagged-1 (JAG) was employed to verify whether CSF2 influences the resistance of CRC cells to 5-FU and OXP by modulating the Notch signaling pathway.
resultsHigh expression of CSF2 is associated with poor prognosis in CRC patients. CSF2 is downregulated in CRC cells that resistance to 5-FU and OXP. Silencing CSF2 inhibits resistance to 5FU and OXP, reduces the survival of resistant CRC cells, and promotes apoptosis. CSF2 activates the Notch signaling pathway, which is highly expressed in CRC resistant cells; conversely, silencing CSF2 inhibits the activation of this pathway. Treatment with JAG reversed the effects of CSF2 silencing on resistance to 5FU and OXP in CRC cells.
conclusionThe silencing of CSF2 inhibited the resistance of CRC cells to 5FU and OXP by regulating the Notch signaling pathway.
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