MCM3 (Minichromosome maintenance complex component 3)

Finally, the adaptability of DepMeta was demonstrated through its successful application in identifying analogous targets in non-small cell lung cancer (NSCLC) and colorectal cancer (CRC). This research proposes DepMeta as a promising tool for identifying essential pan-cancer genes with stable prognostic value, suggesting a foundation for future development of targeted therapies and personalized treatment strategies.

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

The differentially expressed genes associated with the ZMIZ2/MCM3 axis were significantly enriched in multiple pathways, such as the mitogen-activated protein kinase (MAPK), mechanistic target of rapamycin (mTOR), Wnt, and Ras signaling pathways, as verified by The Cancer Genome Atlas data...ZMIZ2 promoted the development by positively regulating MCM3 expression. Key pathways, such as the Ras/MAPK, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mTOR, and Wnt signaling pathways, may be key downstream mechanisms.

In neutrophils, Click-CLOZ bound proteins included MPO, S100, and DEFA1B, which are also associated with neutrophil-mediated oxidative stress and immune responses. In conclusion, the application of click chemistry proteomics has facilitated a novel approach to identify multiple clozapine-bound protein targets that will be used to advance our understanding of the toxicity of clozapine.

Molecular docking results revealed that, compared to norcantharidin, GLA exhibited distinct binding energy (-7.6 vs -6.4 kcal/mol) and a different binding mode with CDC6, supporting its potential as a novel CDC6 inhibitor. These findings provide valuable insights into the potential therapeutic application of GLA for TNBC treatment.

Our data provide new relevance for neovascular inflammatory vitreoretinopathy (NIV), a progressive eye disease caused by pathogenic mutations in CAPN5. Data are available via ProteomeXchange with identifier PXD064313.

In this study we identified the common DEGs of ENKL and EBV infections, found 14 hub DEGs that may mediate between them. Hope this study could provide new insights for further study of the molecular mechanism between EBV infection and ENKL.

Furthermore, RNA-seq has revealed the impact of LINC00880 on the cell cycle and DNA replication pathways, and identified MCM3 as a potential downstream target of LINC00880. Our findings indicate that LINC00880 is upregulated in CRC and promotes tumor growth.

These findings revealed a novel mechanism by which p53 deficiency or mutation drives tumor progression via HNRNPCK189Cr through MDM2/HDAC3 axis-mediated CCND1 and MCM3 mRNA stability. Targeting HNRNPC and its crotonylation with sodium phytate and HNRNPC siRNA offers a promising therapeutic strategy, potentially converting p53 from an "undruggable" target to a "druggable" target.

In conclusion, the synergistic effects of RAM and 5-Aza in HCC cells are mediated through increased damage to DNA, apoptosis, and arrest of cell cycle, offering potential treatment strategy for advanced HCC. Further experiments conducted in vivo are warranted to validate these findings and optimize treatment regimens.

Moreover, in vitro and in vivo experiments further confirmed that MCM3 could promote the proliferation of HCC by regulating cell cycle progression. Our results indicated that MCM3 was up-regulated in HCC and might become a biomarker in the diagnosis and treatment of patients with HCC.

MCM3 emerges as an oncogenic influencer in HCC, driving disease progression through the AKT/Twist axis. Its expression patterns hold prognostic value, and targeting MCM3 may offer a novel therapeutic strategy for HCC.