CEBPZ (CCAAT Enhancer Binding Protein Zeta)

p value < 0.0001), and pancreatic cancer-diabetic (log2FC = 2.73, adj. p value < 0.0001) groups compared to the control group.For the first time, this study suggested that CEBPZ expression may serve as a diagnostic biomarker for assessing PDAC in individuals with T2D, given its differential expression in this specific cohort.

Our study revealed, for the first time, that BA ameliorated liver fibrosis by directly targeting CEBPZ, disrupting its LLPS, and activating the p53/HK2 axis to induce HSC senescence. This work uncovered a novel plant-derived therapeutic strategy targeting a previously unrecognized CEBPZ-LLPS/p53/HK2 mechanism in hepatic fibrosis.

In conclusion, NSUN6 promoted GC progression by stabilizing CEBPZ mRNA in an m5C-dependent manner. However, further in vivo and clinical studies are warranted to validate these findings and explore their translational potential.

Moreover, comparative analysis of TCGA datasets from tumor databases revealed that CEBPZ, NOC2L, and NOC3L exhibit contrasting expression patterns across tumor types. This context-dependent behavior suggests that overexpression of these proteins may promote tumor growth, whereas reduced expression could exert tumor-suppressive effects, underscoring their complex and unexpected regulatory roles in cancer.

Experimental validation with RT-qPCR confirmed the differential expression of the candidate biomarkers (ARRB1, RPS3A, COL4A5, COL1A2 and MED10) across the three CRC stages reinforcing their potential as stage-specific biomarkers in CRC progression. These findings provide a foundation to distinguish between the CRC stages and for the development of accurate stage-specific diagnostic and prognostic biomarkers, which helps in the development of more effective therapeutic strategies for CRC.

Lomustine and hydralazine emerged as potential candidate drugs for treating polycythemia. Abdominal breathing training for three months improved symptoms and reduced RBC, HGB, and HCT in 33 HAP patients. These findings elucidate HAP's molecular mechanisms and suggest new therapeutic directions.

Loss of RB1 has been recently detected in two PRRX1-rearranged mesenchymal tumors on immunohistochemistry and FISH analysis,7 suggesting a potential overlap with RB1-deficient soft tissue tumors. As an emerging entity, PRRX1-rearranged mesenchymal tumors have not been included (yet) in the publication of the 2020 World Health Organization classification of soft tissue and bone tumors.8.

Comparative analysis of their expression in tumor databases revealed that CEBPZ, NOC2L, and NOC3L exhibit contrasting expression patterns across tumor types. This dual role suggests that their overexpression promotes tumor growth, whereas reduced expression may exert tumor-suppressive effects, uncovering unexpected regulatory functions exerted by these proteins in cancer.

Much higher induction of Cidea mRNA was seen in the liver of Cbfa2t3-/- mice after WY14643 administration. These results indicate that hepatic CBFA2T3 is a PPARA-sensitive gene that may modulate metabolic stress in mouse liver.

By targeting Tspan15 to block ADAM10 activity on N-cadherin, GW501516 could prevent NTF pro-tumoral effects and be a promising molecule to treat bladder cancer. More interestingly, it could optimize the effects of the N-cadherin antagonists those such as ADH-1 that target the N-cadherin ectodomain.

Thus, unlike thapsigargin and tunicamycin, which induce ER-stress indiscriminately, PIKFYVE inhibitors selectively terminated PIKFYVE-sensitive melanoma by inducing IL24-dependent ER-stress. Moreover, induction of cell death by a PIKFYVE inhibitor together with ectopic expression of IL24 protein was cumulative, thereby confirming the therapeutic potential of PIKFYVE inhibitors in the treatment of melanoma.

Our findings identified novel FTLD-associated loci, including OTUD4 , and point to DNA methylation as an important mechanism in the dysregulation of biological processes relevant to the FTLD pathogenesis, such as RNA/stress granule formation.