NUDT1 (Nudix Hydrolase 1)

Such inhibition aims to exploit cancer cell vulnerabilities by increasing the accumulation of damaged nucleotides and enhancing susceptibility to DNA-damaging agents (e.g., chemotherapy, radiotherapy) or PARP inhibitors, offering promising avenues for novel combination therapies. This review comprehensively overviews the mechanisms, diverse functions, and pathophysiological roles of NUDT in cancer biology, critically evaluating their therapeutic potential and the challenges in targeting them.

This study uncovered crucial genes shared between pSS and CKD, shedding light on their co-morbidity mechanisms and possible diagnostic biomarkers. Key Points • This study unveils for the first time the immunological association between PSS and CKD. • NUDT1 and COMMD2 are identified as key molecules in the comorbidity mechanism of PSS and CKD. • A diagnostic model for the comorbidity of PSS and CKD is constructed.

Here, we summarize all available research on MTH1 mRNA, protein and its enzymatic activity in clinical samples across various cancer types, identifying a subset of cancers where MTH1 plays an important role. This is particularly evident in cancers characterized by high metabolic activity and oxygen-rich environments, such as hepatocellular carcinoma, renal cell carcinoma, or non-small cell lung adenocarcinoma.

Our research emphasises the role of NUDT1 in modulating the intestinal microbiota and intestinal mucosal barrier in UC, indicating that targeting NUDT1 during intestinal mucosal inflammation could serve as a promising therapeutic strategy for UC.

Using bioinformatics, this study identifies key factors associated with NM in GBM that may influence patient prognosis. This study enhances our understanding of GBM, provides valuable insights for further research, and serves as a reference for evaluating patient outcomes.

The proliferation and cytotoxic activity of T cells were maintained under hypoxic conditions, and PD-1 blockade further augmented the cytotoxicity. These results indicate that MTH1-targeted immunotherapy combined with checkpoint blockade can be an effective strategy for the treatment of hypoxic tumors.

NUDT1 silencing can inhibit the proliferation of tumor cells and increase the production of intracellular ROS to further improve the efficacy of SDT. Then, si-NUDT1 assembled with PT2 and DSPE-PEG-FA to prepare a novel tumor-targeting nanodrug (PT2-siRNA@PEG-FA) for synergic SDT and gene therapy of HCC.

Altogether, we identify AP-2α as a crucial transcription modulator in HCC and propose small-molecule inhibitors targeting AP-2α are a promising novel class of anticancer agents. Our study provides insights into the concept of macroscopic inhibition of DNA damage repair-related genes in cancer treatment.

Administration of LC-1-40 elicits excessive nucleotide oxidation, cytotoxicity and therapeutic responses in patient-derived xenografts. Thus, pharmacological targeting of NUDT1 represents an actionable MYC-driven metabolic liability.

Knockdown of LSM1/NUDT5 could restrain the malignancy of HNSCC cells. Collectively, quantitative assessment of m7G modification patterns in individual HNSCC patients could contribute to identifying more efficient immunotherapeutic approaches and improve the clinical outcome of HNSCC.

Higher Fn in HPSCC patients suggests poorer prognosis. NUDT1 might affect cell proliferation and autophagy and modulate DNA damage response. The oxidative stress induced miR-361-3p/NUDT1 axis is first introduced in microbiome-carcinoma research.