CUL4B (Cullin 4B)

In vivo experiments have demonstrated that MAZ knockdown inhibits tumorigenesis and metastasis in mice. Our findings highlight a novel mechanism wherein MAZ plays a transcriptional inhibitory role by recruiting HDAC1 to catalyze histone deacetylation, and the MAZ/HDAC1 complex inhibits CSK expression, thus promoting tumor proliferation and metastasis.

This study provides novel insight into the role of cullin genes in READ, suggesting that CUL2 and CUL7 may be biomarkers and therapeutic targets. Further research is warranted to explore their underlying mechanisms and clinical applications in READ management.

Furthermore, MLN4924 sensitizes ccRCC to γ-glutamylcysteine synthetase inhibitor Buthionine sulfoximine (BSO) treatment in vivo. Collectively, these findings proposed that MLN4924 could inhibit the tumor growth of VHL deficiency-driven ccRCC by stabilizing FBP1, providing new target and strategy for clinic treatment of ccRCC.

Besides that, circ_0003520 also hindered tumor growth In Vivo via miR-205-5p/CUL4B axis. Circ_0003520 acts as an oncogene to promote ccRCC progression by regulating the miR-205-5p/CUL4B axis, indicating a promising strategy for suppressing ccRCC growth.

In metabolic diseases, CUL4B regulates adipose tissue and insulin sensitivity, with its depletion improving metabolic phenotypes. This review highlights the pivotal role of CUL4B in maintaining immune homeostasis and provides novel perspectives and insights into the understanding and development of treatments for immune-related disorders.

CUL4B was crucial in driving tumor advancement and inhibiting differentiation in TC by facilitating the ubiquitin-mediated degradation of ARID1A, underscoring its potential as a therapeutic target.

The non-m5C carcinogenic roles of NSUN2 may be mediated through interactions with CUL4B, thereby activating the ErbB-STAT3 signalling pathway. NSUN2-mediated upregulation of ErbB-STAT3 pathway enhances the sensitivity of CRC to lapatinib treatment.

In addition, mRNA and protein levels of Bhmt1b are elevated in the liver of RAD52KO mice. Taken together, this study provides valuable insights into the function and mechanism of RAD52.

A missense CUL4B variant c.838 T > A associated with 46, XY female DSD was identified, and may activate the Wnt4/β-catenin pathway. Our findings provide novel insights into the molecular mechanisms of 46, XY female DSD.

In summary, the fitness benefit of TP53 and KRAS mutations was not treatment-related, unlike patient-derived drug resistance alterations that may only induce an advantage under treatment. CCAs are suitable models for the study of clonal evolution and competitive (dis)advantages conveyed by a specific genetic lesion of interest, and their dependence on external factors such as the treatment.

CUL4B downregulation promotes the apoptosis of lens epithelial cells. Our study may help in understanding the role of CUL4B in ARC pathogenesis.