RNF114 (Ring Finger Protein 114)

These data elucidate the negative regulatory mechanism involving the VP2-RNF114-IKBKE/IKKε-CALCOCO2 axis, and reveal an immune evasion strategy employed by picornaviruses. These findings will provide valuable insights for the development of picornaviral vaccines and antiviral/antitumor therapeutics.

Distinctive features of this study include pharmacology-focused tagging of E3 ligases (e.g., CRBN, DCAF15, RNF114), neosubstrates (IKZF1/3, RBM39, BRD4), and translational signals (clinical-phase and patient-linked studies). By capturing 2024 publications and providing therapeutic and mechanistic stratifications, this analysis complements earlier bibliometric studies and highlights opportunities for global collaboration, disease diversification, and translational development of molecular glues.

We hypothesize that other chloro-N-acetamide-containing E3 ligase ligands would also induce ferroptosis. Indeed, the RNF114 ligand EN219 also strongly induces ferroptosis, suggesting that ligands harboring this electrophile induce undesired off-target toxicity.

Extensive research has demonstrated that RING-UIM E3 ligases fulfill specific biological roles in carcinogenesis by ubiquitinating critical oncogenes and tumor suppressors, thereby modulating various signaling pathways, differing their functions across distinct cancer contexts. This review comprehensively examines the multifaceted roles of RING-UIM E3 ligases in human cancers, elucidates the molecular mechanisms underpinning their actions and regulatory effects on cancer cells, and explores their potential clinical applications.

Additionally, RNF114 is implicated in multiple diseases, such as viral infections, psoriasis, liver fibrosis, and cancer. This review recapitulates the most recent advances regarding RNF114 and provides possible directions for future research.

And knockdown of RNF114 suppresses proliferation, migration, invasion, and autophagy of HER2-positive BC cells. Our findings highlight the transcriptional regulatory function of RNF114 in BC, offering new insights into its oncogenic role and contribution to HER2-positive BC progression.

Overall, this study reveals that circFADS1 regulates GSK3β function, influencing the progression of hepatocellular carcinoma. The EIF4A3/circFADS1/GSK3β/β-catenin axis is discovered to hold promise as a novel therapeutic target for hepatocellular carcinoma, while circFADS1 is also a significant factor in lenvatinib resistance.

In summary, elevated SPP1 expression was associated with poor clinical outcomes in NSCLC patients. This study highlights the role of SPP1 as a regulator of cell metastasis and suggests its potential as a novel therapeutic target for BM in NSCLC.

XAF1 expression is inversely correlated with TRIM28 expression in cancer cell lines and tumor tissues and more tightly associated with the survival of TRIM28-high versus TRIM28-low patients. Together, this study uncovers a novel mechanism by which XAF1 suppresses tumor malignancy and an important role for XAF1-TRIM28 interplay in governing stress response, illuminating the mechanistic consequence of its alteration during tumorigenic process.

Through a sulfonyl hydrazone-mediated etherification and a radical cyclization, this strategy uses a pharmacophore-containing building block and diversifiable hydrazone units to enable the modular synthesis of nimbolide and its analogues. The broad generality of our synthetic strategy allowed access to a variety of analogues with their preliminary cellular cytotoxicity and PARP1 trapping activity reported.

In mice with tumours, the injection of cytotoxic T cells collected from the animals and treated with a PIEZO1 antagonist promoted their infiltration into the tumour and attenuated tumour growth. As an immunomechanical regulator, PIEZO1 could be targeted to enhance the outcomes of cancer immunotherapies.

Moreover, we observe correlations between the protein levels of XAF1, RNF114, and JUP in clinical samples. Collectively, our findings reveal an oncogenic function of XAF1 in mCRC and suggest that the XAF1-VCP-RNF114-JUP axis is a potential therapeutic target for CRC treatment.