MZF1 (Myeloid Zinc Finger 1)

MZF1-AS1 strengthens the interaction between NSUN2 and RAB13 mRNA, promoting NSUN2-mediated m5C modification and stabilizing RAB13 mRNA. Our findings uncover a novel epi-transcriptomic mechanism by which MZF1-AS1 promotes GC progression via NSUN2-dependent m5C methylation of RAB13 mRNA, offering new insights into PM pathogenesis and highlighting potential therapeutic targets for advanced GC.

Collectively, these findings demonstrate that miR‑199a‑3p suppresses NSCLC progression by targeting FTO, promoting m6A methylation‑dependent downregulation of MZF1, and consequently decreasing CLDND1 expression. Thus, the miR‑199a‑3p/FTO/MZF1/CLDND1 axis may serve as a promising therapeutic target in NSCLC.

Moreover, based on our EGFP reporter assay, we conclude that the regulatory region of the PRAME locus-without PRAME transcription-is insufficient to drive transcription of PRAME-AS in the antisense direction. Taken together, our data support the conclusion that PRAME-AS lncRNA acts as a regulator of PRAME transcript levels, and that MZF1-and the methylation status of a shared CpG island- influence the expression of both genes.

Collectively, these findings underscore the pivotal role of MZF1 in tumor biology and immune modulation. MZF1 emerges as a promising prognostic biomarker and potential therapeutic target, offering novel avenues for cancer treatment strategies.

Constructs V1 and V5 demonstrated superior immunogenicity and TLR binding, while V2 and V5 induced strong immune responses in silico. These findings provide a foundation for developing effective peptide vaccines against TNBC.

ScRNA-seq revealed the heterogeneity of HNSCC subpopulations, highlighting the unique features of the C2 MALAT1+ Tumors subpopulation. This study identified novel prognostic markers and therapeutic targets, offering insights into HNSCC progression, drug resistance, and potential treatments.

Sumoylated MZF1 can interact with proteins containing SUMO-interaction motifs (SIM) through SUMO-SIM interaction. Interactome analysis revealed that its NBs participate in the stress response (TPR and UBAP2L), protein folding (CALR and ANKRD40), transcription, post-translational modification (TRIM33, ACOT7, CAMK2D, and CAMK2G), and RNA binding (ALURBP and CPSF5).

CHD-associated biomarker ZNF429 was identified through bioinformatics analysis to potentially regulate the expression of inflammatory factors IL-6, IL-1β, and TNF-α, along with adhesion molecules ICAM-1, VCAM-1, CD62E, and CD62P. This modulation influence was subsequently found to impact the progression of CHD. These findings offered valuable insights into potential targets for further investigation and therapeutic interventions for CHD management.

In conclusion, cigarette smoke significantly influences the development and progression of oral squamous cell carcinoma, based on the evidence highlighted in human oral cells. While previous studies have focused on specific carcinogens and pathways, this review added to our understanding of the overall impact of whole cigarette smoke on oral carcinogenesis at the molecular and cellular levels.

Finally, we demonstrated the interaction between SIRT6 and MZF1 using ChIP-qPCR. In conclusion, mitoAMPK inhibits the Warburg effect by regulating the expression of the MZF1-SIRT6 complex.

The fluorescence relative expression of each mutant was detected by Renilla luciferase assay. By binding to MZF1 (Myeloid zinc finger protein 1, MZF1), Solamargine inhibits HBV core promoter activity, reduces pregenomic RNA level, and inhibits HBV, achieving antiviral effects.

The results suggest that MZF1 may be involved in osteoclast differentiation by regulating RANKL-induced ferroptosis of osteoclasts. Collectively, our findings shed light on the essential involvement of MZF1 in the regulation of osteoclastogenesis in osteoporosis and provide insights into its potential underlying mechanism.