MCM10 (Minichromosome Maintenance 10 Replication Initiation Factor)

The differential expression of SSP genes suggest a potential molecular contribution to CRC disparities in the Hispanic population. The essential oncogenic role of MCM10 and its axis with PPFIA1 was identified; this could lead to a new avenue for therapeutics targeting the MCM10-PPFIA1 axis, thereby, combating early-onset and advanced-stage CRC in this high-risk ethnic group.

These findings suggest that MCM10 may be a potential prognostic biomarker for ACC and may provide new insights into its role in tumor biology. Further studies are needed to elucidate the therapeutic significance of MCM10 and its mechanistic involvement in ACC progression.

MCM 10 is a key mediator of TMZ resistance in glioblastoma.

Metformin and everolimus are synergistic in anticancer effects on RCC. Based on transcriptomic data, this study obtained five hub genes associated with everolimus and metformin combination therapy in KIRC to inform KIRC-related research.

These findings reveal that MCM10 promotes CRC malignancy through inhibiting the tumor-suppressive p53/p21/CCND1 pathway. Targeting this axis, particularly through ultrasound-enhanced delivery or sensitization strategies, holds promise as a novel therapeutic approach in CRC.

MCM10 plays a pivotal role in promoting cancer stemness and sorafenib resistance in HCC. Targeting MCM10 transcription with TW-37 represents a novel strategy to overcome sorafenib resistance and improve therapeutic outcomes in HCC patients.

Methionine deprivation through MEGL-targeted gene therapy may be a viable option for inducing cancer cell death compared to unrestricted levels of methionine.

Targeting METTL3 O-GlcNAcylation with designed peptides effectively inhibits HCC growth both in vitro and in vivo. Collectively, our findings provide insights into the regulatory role of O-GlcNAcylation in modulating the m6A epitranscriptome and suggest the potential therapeutic relevance of targeting METTL3 O-GlcNAcylation in HCC.

Correlation analysis revealed that a MAGI2-AS3/hsa-miR-450b-5p/COLEC10 axis might play a crucial role in the progression of HCC. The ceRNA network constructed could provide insight into HCC tumorigenesis and might lead to new molecular biomarkers for diagnosing and treating HCC.

Due to its binding at the origin-promoter locus like the MCM4 gene, ETV4 overexpression increases R-loop formation, DNA damage, and cell death under external replication stress induced by topoisomerase I (TOP1) inhibitor. These findings highlight the dual role of ETV4 in replication and transcription and suggest that targeting TOP1 could be a synthetic-lethal approach in ETV4-overexpressed lung cancer.

RT-qPCR confirmed significant upregulation of MCM10, KIF18A, CDC45, and PLK4 in HCC tissues (p< 0.05). This study successfully identified eight prognostic genes (MCM10, CEP55, KIF18A, ORC6, KIF23, CDC45, CDT1, and PLK4), which provided new directions for exploring the potential pathogenesis and clinical treatment research of HCC.

Moreover, we discovered that RAD51 and its main co-expressed genes were significantly negatively associated with most or all immune cell infiltration. RAD51 overexpression was related to disease progression and poor prognosis, as well as infiltration of immune cells in gastric cancer.