SMURF2 (SMAD Specific E3 Ubiquitin Protein Ligase 2)

In addition, resistance to existing cancer therapy related to SMURF2 and sensitivity mechanisms is discussed. Lastly, theranostic strategies for anticancer agents and biomarker development are suggested.

NLRP3 neddylation hinders its interaction with Trim31 and thereby inhibits its K48-linked ubiquitination and subsequent degradation. MLN4924, a potent compound NAE inhibitor in phase 1/2/3 clinical trials for cancers, alleviates psychological stress-induced NLRP3 inflammasome activation, microglia inflammatory activation, and anxiety-like behavior, suggesting novel clinical activity of MLN4924.

These findings contributed to our understanding of the molecular mechanisms underlying the maintenance of the stemness and tumorigenicity of GSCs through protein posttranslational modifications. We propose that these two protein posttranslational modifications in GSCs might be explored as an effective therapeutic approach against various cancers whose malignancies are associated with the stemness of cancer stem cells.

These findings could pave the way for more effective immune-based treatments and improve the prognosis for OC patients. Future research should focus on validating these biomarkers and exploring their functional roles in OC pathogenesis and treatment response.

Strikingly, the downregulation of Smurf2 promotes cell viability through CASC3, while overexpression of Smurf2 retards tumor growth in mouse models. Collectively, our results suggest that the Smurf2/CASC3 axis may serve as a potential therapeutic target for the treatment of leukemia.

SMURF2 plays a key role in OC by inhibiting cell autophagy and growth via activation of the RACK1/AKT/mTOR pathway, which might potentially be a new biomarker for OC diagnosis and therapy.

Molecular docking studies support curcumin's direct binding to several pyroptosis-associated proteins, including NLRP3, AMPK, caspase-1, and Smurf2. These context-dependent regulatory effects underscore the therapeutic potential of curcumin as both an inflammasome suppressor in inflammatory diseases and a pyroptosis inducer in cancer.

Additionally, combining copper chelators with anti-PD-1 treatment effectively suppresses tumor growth, and high levels of SLC31A1 are notably associated with non-response to anti-PD-1 treatment. In conclusion, the crucial role of copper in modulating EZH2 protein stability is demonstrated, and a new approach using copper chelators and anti-PD-1 therapy for OSCC patients is provided.

We discovered that MNX1-AS1 is significantly elevated in BC and contributes to paclitaxel resistance through the PI3K/AKT pathway...These findings underscore the role of MNX1-AS1 in activating the ITGA6/PI3K/AKT pathway, which facilitates tumor progression and induces chemoresistance in BC. Targeting MNX1-AS1 may represent a promosing therapeutic strategy to enhance chemotherapy efficacy in BC patients.

Inhibition of SMURF1 expression suppressed the proliferation and migration of pancreatic cancer cells. High expression of SMURF1 could potentially be a therapeutic target and a poor prognostic indicator in pancreatic cancer.

Our findings suggest that FGR is associated with a down-regulation of MYO1A, which may affect the Hh pathway through its interaction with SMURF2. This provides clues for a deeper understanding of the specific mechanisms underlying FGR.

In comparison, J-1156 demonstrated superior overall therapeutic efficacy to J-1155 in terms of anti-fibrotic efficacy, while J-1155 exhibited superior modulation of Smurf2. Collectively, our observations demonstrate the potential of J-1155 and J-1156 as dual novel therapeutic agents targeting hepatic fibrosis.