CUL4B (Cullin 4B)

Clinically, ccRCC patients with high DR5 expression show decreased responsiveness to TKI-based therapy. Collectively, these results highlight the importance of the positive feedback loop involving the DR5/NF-κB axis in sunitinib resistance and provide an effective therapeutic strategy for overcoming resistance.

PRMT5-mediated Sohlh2 arginine methylation promotes the CUL4B-mediated ubiquitylation and degradation of Sohlh2, leading to the inhibition of Sohlh2 effects in VECs. Taken together, these findings demonstrate that PRMT5/Sohlh2/Sirt1 signaling pathway in VECs plays a critical role in regulating the lung metastasis in TNBC, indicating PRMT5/Sohlh2/Sirt1 signaling as potential targets in the treatment of TNBC metastasis.

KDM5B upregulation was significantly negatively correlated with the survival rates in various cancer types, including thyroid, lung, esophageal and colorectal cancers. Overall, these findings establish a novel regulatory axis in cholesterol metabolism, uncover potential therapeutic vulnerabilities in ER+ breast cancer, and suggest that targeting the KDM5B could provide a strategy to curb tumor progression.

Our study elucidates the tumor-suppressive role of GATA4 in regulating lysosomal acidification and epithelial-mesenchymal transition through ubiquitination-dependent mechanisms and histone acetylation modulation. The findings identify GATA4 as a promising therapeutic target and diagnostic marker for ovarian cancer intervention.

We define three molecular subtypes with distinct outcomes and present an integrative machine learning model combining clinical, genomic, and proteomic features, validated in an independent test dataset of 105 patients and a published dataset. This multi-center, multi-omics study enhances the understanding of MTC heterogeneity and facilitates personalized patient management.

Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 17: 4973‑4980, 2018; DOI: 10.3892/mmr.2018.8509].

This reduction impairs miR-143-3p formation, activates the KRAS signaling pathway, and promotes tumor progression and oxaliplatin resistance. In summary, this study provided compelling evidence that CUL4B knockdown may be a promising strategy for treating HCC and increasing tumor cell sensitivity to oxaliplatin therapy.

Notably, JAB1 inhibition reverses chemotherapy resistance associated with CUL4B overexpression. These findings underscore the pivotal role of JAB1 in regulating breast cancer progression and indicate that JAB1 inhibitors could serve as promising therapeutics for patients with elevated CUL4B expression.

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.