CBX8 (Chromobox 8)

Overall, CBX8 phosphorylation by PKD1 impaired PRC1 complex integrity and activity, mitigated H2AK119ub1 level, caused the upregulation of multiple target genes repressed by CBX8, and decreased CBX8, H2AK119ub1, and H3K27me3 enrichment at INK4A/ARF locus, thereby derepressing p16INK4A and facilitating cellular senescence. Collectively, these results suggest that PKD1-mediated CBX8 phosphorylation at T234 and S256/311 is a key mechanism governing CBX8 function, including cell senescence.

These findings point to a potential interplay between CBX4 and inflammation-related pathways in CC. Overall, our study highlights the oncogenic role of CBX4 in colorectal cancer and supports its potential as a novel therapeutic target and early biomarker for disease progression.

Furthermore, we confirmed the prognostic significance of TMEM18 expression at the protein level with immunohistochemistry (IHC) in a primary PCa tumor cohort. In conclusion, we identified 85 mCRPC-associated genes and showed that TMEM18 has prognostic value in early PCa.

Targeting PLK1 enhances BRAFi ± EGFRi inhibition and triggers ferroptosis in vitro, vivo, organoid, and patient-derived xenograft model. Collectively, we demonstrate a PLK1-CBX8-GPX4 signaling axis that relays the ferroptosis mechanism of therapeutic resistance and propose a clinically actionable strategy to overcome BRAFi ± EGFRi resistance in BRAFV600E CRC.

In pyroptosis, LRRFIP2 and FLII which can inhibit pyroptosis increasingly binding to MST1. Our findings delineate potential mechanisms through which MST1 and its interactomes regulate cell death, paving the way for further investigation to validate and consolidate these observations.

Gene expression and immune cell infiltration were different in tissues stratified by miR-187 expression. In summary, the integration of differential gene expression, co-expression analysis, and immune cell profiling provided insights into the molecular intricacies of GC progression.

Exosomal miR-127-3p further stimulates M1 polarization of macrophages by suppressing ZC3H4. Taken together, the detailed understanding of the mechanisms through which β-elemene induces autophagy in NSCLCs and facilitates M1 polarization of macrophages provides compelling scientific evidence supporting its potential utility in NSCLC treatment.

Mouse CNV was lessened by the blockade of CBX7 through the down-regulation of HIF-1α/VEGF. In conclusion, CBX7 enhanced pro-angiogenic behaviors of hypoxic CVECs by up-regulating the HIF-1α/VEGF pathway, which contributing to the formation of mouse laser-induced CNV.

CBX2 is involved in the development and advancement of PCa, suggesting its potential as a reliable prognostic indicator for PCa patients.

To target, reprogram, and kill leukemic cells, we suggest and describe multiple therapeutic strategies to interfere with the epigenetic functions of oncogenic CBX proteins. Future studies should clarify to what extent the non-epigenetic function of cytoplasmic CBX proteins is important for normal, aged, and leukemic blood cells.

Also, CBX8 expression could be modulated by circSPECC1 via miR-1236-3p regulation. Collectively, we indicated that inhibiting circSPECC1 could suppress growth and promote apoptosis of BC cells in both irradiated and nonirradiated conditions at least partially via miR-1236-3p/CBX8 axis, confirming that circSPECC1 might be target to develop anticancer drug in BC.

Collectively, these data demonstrated that CBX8 induced EMT through Wnt/β-- catenin signaling, driving migration and invasion of LC cells.