UBE2D3 (Ubiquitin Conjugating Enzyme E2 D3)

Furthermore, combining an UBE2D3 small-molecule inhibitor with KRASG12D-specific TCR-T-cell therapy yields synergistic antitumor effects. Our findings reveal a negative feedback mechanism in which cancer cells, "camouflaging" themselves, evade IFN-γ-induced antigen presentation via UBE2D3 upregulation, highlighting a potential therapeutic target for enhancing antitumor immunity.

Cuproptosis represents a novel mechanism dependent on copper that has important implications for the treatment of lung cancer. This process primarily involves the buildup of copper ions, which leads to a disruption in protein homeostasis, ultimately resulting in cell death. Additionally, the abnormal expression of crucial regulatory genes, such as FDX1 and LIPT1, along with transport proteins like CTR1 and ATP7A/B, is closely linked to the advancement of lung cancer. At present, drugs that act as carriers for copper ions (such as elesclomol and disulfiram), metal-organic frameworks based on copper, and copper chelators (including D-penicillamine and ammonium tetrathiomolybdate) have demonstrated promise in eliciting copper-mediated cell death in lung cancer cells. These discoveries suggest new potential targets and strategies for treating lung cancer, which could enhance the prognosis for patients diagnosed with the disease.

The six neddylation-related genes (CUL1, PUM2, UBE2D3, HIF3A, COPS2, and DDB1) emerge as potential independent indicators of survival in patients with BLCA, and the constructed survival models exhibit significant diagnostic efficacy.

And this was confirmed by siRNA-mediated gene knockdown in inflammatory macrophages. Our results suggested that EB may be a new kind of UBE2D3 inhibitor and may become a promising therapeutic agent for anti-periodontitis.

This study presents a novel three-gene prognostic model based on UBE2RGs that demonstrates significant predictive value for OS, immunotherapy, and chemotherapy in ccRCC patients. The findings underscore the potential of UBE2 family members as biomarkers and therapeutic targets in ccRCC, warranting further investigation in prospective clinical trials.

Furthermore, our findings revealed that WTAP promotes the m6A modification of UBE2D3 via an IGF2BP1-dependent mechanism. The WTAP-IGF2BP1 axis regulates UBE2D3 stability in an m6A-dependent manner, influencing tumor malignancy and TMZ chemosensitivity in GBM via the DNA repair signaling pathway.

This study demonstrates a rare correlation between a chromosome 4q abnormality and HGSC. UBE2D3 may affect crucial cancer-related pathways, including P53, BRCA, cyclin D, and tyrosine kinase receptors, thereby possibly contributing to cancer development. In addition, ADH1 and DDIT4 may be potential influencers of both carcinogenic and therapeutic responses.

Our work identifies a novel IRE1/UBE2D3 pro-inflammatory axis that plays an instrumental role in GB immune regulation.

These data suggested a mechanism through which the linear ANRIL transcript P14AS can promote inflammation and colon cancer progression through the sequestration of miR-23a-5p and the modulation of NF-κB signaling activity, thus highlighting P14AS as a promising target for therapeutic intervention efforts.

DβH, UBE2D3, SOD1, UBE2D1, and LOXL2 are potential candidates implicated in LUAD and can be further explored for their application as diagnostic, prognostic, and therapeutic biomarkers for LUAD.

Two mutations (BRCA1 and BARD1) hindered significant interaction between protein partners and may prevent signaling for ubiquitination of histones in NCP and other cellular targets. The structural compactness and reduced significant interaction in mutant complexes may be the possible reason of preventing ubiquitination and hinder DNA repair, resulting cancer.