CBX3 (Chromobox 3)

WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

Clinically, CBX3 expression was significantly correlated with TNM stage and was predictive of both progression-free interval and overall survival in LUAD. In a prospective cohort of LUAD and melanoma patients, CTCs co-expressing CBX3 and GPX4 were selectively elevated in the blood samples of metastatic cases compared to the non-metastatic group, highlighting the clinical association between ferroptosis-resistant CTCs and metastatic progression.

Our study established lactylation modifications as a crucial regulator of the TME and glioma progression. Through integrative multi-omics analysis and robust machine learning techniques, we determined that RAN was a novel lactylation-associated gene. RAN is a potent, independent prognostic biomarker that promotes glioma malignancy via the PI3K/AKT pathway. Our results demonstrate RAN as a prospective therapeutic target and establish a novel framework for individualized therapy for glioma.

The results of the study demonstrated the involvement of HP1 in the DDR via covalent PARylation by PARP1, resulting in the suppression of transcription and the promotion of HR repair. Overall, these results identify a new molecular mechanism of DNA damage-induced transcriptional repression and provide a theoretical basis for the potential application of DNA damage-induced transcriptional repression in the treatment of osteosarcoma.

Fusion cells accumulated abundant intracellular lipid droplets and were highly sensitive to simvastatin treatment in vitro and in vivo. Together, this study uncovered that CBX3-SNX10-ANO6 signaling facilitates generation of an aggressive tumor-LAM fusion cell subpopulation that promotes metastasis, revealing an alternative metastatic mechanism and exposing putative therapeutic vulnerabilities. Single-cell transcriptomic profiling combined with functional and clinical validation identifies fusion of tumor cells and lipid-associated macrophages mediated by the CBX3-SNX10-ANO6 axis as a potentially targetable mechanism driving cancer metastasis.

CDX2 overexpression enhanced migration, invasion, and xenograft growth, whereas CBX3 knockdown suppressed these phenotypic changes. In conclusion, this study defines clinically relevant CBX molecular subtypes in LUAD and reveals the CDX2-CBX3 transcriptional cascade as a novel driver of tumor progression, offering potential targets for precision therapy.

Notably, it exhibited a strong positive correlation with the presence of Fusobacteria, which are also implicated in modulating these pathways. In addition, the glutaryl CoA degradation and p-cymene degradation pathways demonstrated a strong positive association with the expression of the Ahcy, Eis2s2, Hsp90ab1, Psma7, Lbr, Rpl7l1, Cse1l, Cbx3, Ncl, Hspd1, Tpx2, and Top2a genes (r > 0.65), suggesting their potential involvement in the regulation and metabolic integration of these pathways at the transcriptional level.

Knockdown of lncRNA BBOX1-AS1 inhibits U-87 MG cell proliferation and promotes apoptosis by upregulating miR-382-5p and downregulating CBX3 expression.

CBX3 overexpression increased Irinotecan and Oxaliplatin resistance, whereas CBX3 knockdown suppressed multidrug resistance in CRC cells. Our study identified CBX3/NRF2/GPX2 axis may be a novel signaling pathway that mediates multidrug resistance in CRC. This study proposes developing novel strategies for cancer treatment to overcome drug resistance in the future.

Our findings could provide new perspectives for identifying potential prognostic markers within the CBX family in BC. Targeting CBX2 may present a promising approach to address endocrine resistance in BC therapy.

We conclude that the stem cell marker, CBX3 activates the p21/CDK6 pathway and alters the immune microenvironment in melanoma.

All these might exhort differential resistance to treatment. Thus, we found that prognostic and predictive triple biomarkers - KRAS mutated, dual fusions (KMT2A/AFDN, CCDC32/CBX3), and chimeric variants - might evolve with a potential oncogenic role of subclonal evolution for poor clinical outcomes.