MCM7 (Minichromosome Maintenance Complex Component 7)

SETD8 promotes EMT and GC progression primarily by upregulating MCM7 expression, likely via an H4K20me1-dependent epigenetic mechanism. MCM7 acts as a key downstream effector. The SETD8/MCM7 axis represents a novel driver and potential therapeutic target in GC.

By integrating toxicological target prediction with large-scale bladder cancer transcriptomic analyses, this study provides a computational bridge between environmental chemical exposure and cancer-related molecular programs. The resulting nine-gene classifier demonstrates strong and consistent performance across independent cohorts and captures transcriptional features that intersect with PFOA-associated toxicological pathways, offering a systems-level, hypothesis-generating perspective on transcriptional programs that overlap between predicted PFOA-associated targets and bladder cancer biology.

This study demonstrated that NOL6 functions as an oncogene that facilitates CRC progression, suggesting its potential role as a therapeutic target for CRC management.

Actinomycin D treatment and RNase R assay were performed to examine the stability of circMCM7...Notably, overexpression of MCM7 partially rescued the inhibitory effects on proliferation and invasion, as well as the pro-apoptotic effects induced by circMCM7 knockdown. This study elucidates the oncogenic function of circMCM7 in hepatocellular carcinoma and confirms its regulatory roles in HCC cell proliferation, invasion, and apoptosis through modulation of MCM7 expression, suggesting circMCM7 as a potential therapeutic target for HCC treatment.

However, they displayed a dose-dependent inhibition of CDK2 kinase activity in in-vitro ADP-Glo™ assay with IC50 values of 23.47 and 82.04 nM, respectively, compared to 0.51 and 700 nM for Dinaciclib and Roscovitine, respectively. Compound 6 downregulated CDK2 protein targets involved in DNA replication process; Polα, MCM7, ORC2, and ORC4 in CRC cell lines. Subjected to cell cycle analysis, HCT-116 and HT-29 treated with compound 6 demonstrated pre-G1 phase arrest with no similar observation in S phase.

Overall, the lineage-aligned synthesis indicates that NF-PitNETs progress through diverse molecular pathways, with each subtype dominated by distinct regulatory networks. Although many biomarkers show promise, most remain exploratory, highlighting the need for harmonised methods and multicentre validation to support precision diagnostics and prognostic modelling.

This study identified MCM7 and ADAM17 as potential biomarkers for EGC through integrated multi-cohort bioinformatic analysis. Further experimental and clinical studies are required to validate their diagnostic specificity and applicability in real-world settings.

miR-423-5p acts as a tumor suppressor in HCC by targeting key nodes of pro-tumorigenic signalling. miR-423-5p significantly altered metabolic pathways, including purine/pyrimidine metabolism and gluconeogenesis. Seven miR-423-5p targets correlate with poor prognosis in TCGA-LIHC patients and are downregulated in miR-423-5p overexpressing HCC cells. miR-423-5p over-expression induces a significant downregulation of MCM7, DVL3, IMPDH1, SPEE in HCC cell models. miR-423-5p limits tumor metabolic plasticity, suggesting therapeutic potential.

Inhibition of the miR-106b-25 cluster increases caspase-3/7 activity. These findings demonstrate that both MCM7 and the miR-106b-25 cluster contribute to renal cancer progression.

RNA-seq analysis additionally uncovered that SF-153 impaired lysosome acidification and inhibited autophagy to enhance the anti-leukemic activities. Taken together, our study characterized the multimodal mechanisms of inhibition by SF-153 in leukemia cells and laid the foundation for studying selective UHM inhibitors in future.