Fig 1: Correlation analysis was performed to assess the relationships between differentially expressed KDM family genes and immune cell infiltration via the TIMER database. The figure illustrates the associations of KDM1A, KDM5A, and KDM5B gene expression with tumor purity and markers of tumor-infiltrating immune cells, including B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells. Spearman correlations were used to assess the relationships between these KDM genes and the mentioned immune cells, with statistical significance set at p<0.05.
Fig 2: The prognostic value of the mRNA levels of the KDM family in patients with pancreatic cancer (PC) was determined via Kaplan‒Meier plotter analysis. (A) The hazard ratio (HR) indicates the prognostic value for PC patients. The log [rank p] test was used to determine the level of prognostic significance, with a value of p<0.05 considered significant. High expression of KDM1A/5A/5B was significantly associated with poor prognosis, indicating poorer outcomes. Conversely, the HRs of KDM2B/5D/6B were significantly lower, suggesting better prognostic outcomes in patients with pancreatic cancer. (B) Immunohistochemical patterns of KDM1A, KDM5A, and KDM5B expression in normal and tumor tissues from patients with PC.
Fig 3: Expression of the KDM5A signaling pathway in pancreatic cancer (MetaCore). We used the MetaCore platform to analyze genes coexpressed with KDM5A from the associated TCGA database. Our analysis revealed that "DNA damage" was the most common biological process.
Fig 4: KDM5A was up-regulated in osteosarcoma and associated with poor prognosis. A qRT-PCR detected KDM5A level in osteosarcoma tissues, adjacent tissues served as the negative control (n = 58). B IHC detected the number of KDM5A-positive cells in osteosarcoma tissues (five fields of vision, n = 3). C KDM5A protein levels were detected by western blot in 5 out of 58 clinical samples. D The correlation between KDM5A level and overall survival rate of patients (KDM5A high level patients n = 29; KDM5A low level patients n = 29). E qRT-PCR detected KDM5A in osteosarcoma cells, including MNNG, MG63, 143B and SaOS2, hfOB1.19 cells served as the negative control. F Western blot measured KDM5A protein level in osteosarcoma cells, hfOB1.19 cells served as the negative control. * P < 0.05, ** P < 0.01, *** P < 0.001
Fig 5: KDM5A knockdown inhibited osteosarcoma cell proliferation and migration, and promotes apoptosis. sh-KDM5A was transfected into MNNG and MG63 cell for KDM5A knockdown, sh-NC served as the negative control. A qRT-PCR detected KDM5A level. B KDM5A levels were measured by western blot after transfection with sh-KDM5A. C Cell proliferation was detected by colony formation assay. D Cell migration was detected by wound healing assay. E Flow cytometry detected cell apoptosis. * P < 0.05, ** P < 0.01, *** P < 0.001
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