NEIL3 (Nei Like DNA Glycosylase 3)

These findings provide comprehensive characterization of the TME ecosystem in AITL and reveal potential therapeutic targets for high-risk RR AITL patients.

In conclusion, circNEIL3 stabilizes SPI1 mRNA expression by binding to U2AF2, thereby promoting glioma progression and temozolomide resistance. Implications: Our findings offer a new mechanistic insights into gliomas drug resistance, and targeting the circNEIL3/U2AF2/SPI1 axis represents a promising approach to counteract TMZ resistance in gliomas.

This study demonstrates that unsupervised clustering combined with WGCNA and ML enables the discovery of clinically relevant molecular signatures in PCa. Our findings establish TPX2-centered networks together with biological pathways implicated in mitotic regulation and DNA damage repair as key drivers of tumor evolution, providing a biologically informed source for biomarker development, drug testing and mechanistic studies.

FOXM1 could interact with the NEIL3 gene promoter, initiating its transcription. In the context of LUAD, the activation of NEIL3 by FOXM1 constitutes the FOXM1/NEIL3 axis that counteracts ferroptosis in LUAD cells.

In vitro, PCa cell proliferation, invasion, and migration could be significantly inhibited with knocking down NEIL3 by inactivating the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) signaling...In conclusion, NEIL3 could promote the progression of PCa by activating PI3K/AKT/mTOR signaling in PCa cells. Therefore, these results may provide a potential molecular target for PCa treatment.

Additionally, high SF3B6 expression was an independent risk factor for overall survival and correlated with poor alpha-fetoprotein levels, pathological grading, clinical staging, and reduced responses to sorafenib and transarterial chemoembolization treatment in HCC...We emphasize that SF3B6 has the potential to serve as a biomarker for predicting cancer diagnosis, prognosis, and immunotherapy responses, especially in HCC. SF3B6 and its related alternative splicing isoforms promote the occurrence and progression of HCC and may serve as potential therapeutic targets.

Our findings may have important clinical implications for utilizing NEIL3 as a potential prognostic biomarker to stratify EC patients and as a target to enhance immunotherapy response in endometrial cancer. However, our NEIL3 overexpression associated observation still requires further experimental-based scientific validation studies.

Furthermore, knocking down NEIL3 significantly increased the oxaliplatin-mediated inhibition of the Fanconi anaemia pathway. Our results revealed that NEIL3 may be a promising therapeutic target for improving oxaliplatin efficacy in the treatment of HCC.

NEIL3 and TOP2A play key roles in EC progression through the WNT signaling pathway. Targeting these molecules may offer promising therapeutic strategies for EC.

The double knockdown of OGG1 and NEIL1 additively affected the mutation frequency. These results indicated that NEIL1 is another BER protein involved in the action-at-a-distance mutations triggered by the oxidized guanine base.

The 16 key genes identified in this study significantly correlate with PCa stem cell characteristics and showed prognosis-oriented effects in PCa patients. Further, the NUF2 gene may be used as a drug target for treating PCa.

This study suggested that the TFAP2A/NEIL3 axis promoted Mø M2 polarization through Gln metabolism, providing a theoretical basis for immune therapy targeting the liver cancer TME.