APEX1 (Apurinic/Apyrimidinic Endodeoxyribonuclease 1)

The seven hub RBP genes are potential biomarkers for CRC, providing new insights and therapeutic targets. However, functional validation and larger sample sizes are needed for clinical application.

Using A375 and SK-MEL-28 melanoma cells treated with the ferroptosis inducer erastin, we analyzed USP36 expression and evaluated its functional role through both overexpression and knockdown experiments...Collectively, these findings establish USP36 as an oncogene in melanoma that inhibits ferroptosis through stabilization of APEX1. Therefore, targeting the USP36-APEX1 axis may represent a novel therapeutic approach for melanoma treatment.

Histological analysis indicated increased nuclear inclusions and ductular proliferation in both strains, whereas fibrosis was attenuated in Apex1+/- mice. Collectively, these findings show that APE1 is essential for preserving mtDNA integrity and regulating bioenergetics and histopathological responses to alkylation-induced liver injury, highlighting its dual role in mitochondrial maintenance and modulating inflammatory outcomes.

FEN1 rs174538 A>G, FEN1 rs4246215 T>G, APEX1 rs3136817 T>C, and XRCC1 rs25487 C>T are associated with Wilms tumor susceptibility, which provides potential molecular markers for the early diagnosis of Wilms tumor.

Blood samples were collected, and gene polymorphisms were identified using PCR-RFLP technique. Our study results revealed a statistically significant association between gene polymorphisms OGG1-Ser326Cys (p = 0.008), XRCC1-Arg194Trp (p = 0.009), XRCC1-Arg399Gln (p < 0.001), APEX1-Asp148Glu (p < 0.001) and the occurrence of leukoplakia, OSMF and OSCC.

This study identifies key α-HB-related targets and biomarkers for sepsis, offering new insights into its pathophysiology. The findings highlight the potential of α-HB in modulating immune responses and suggest that α-HB-related targets could serve as promising therapeutic targets for sepsis management.

We identified key APIGs and constructed a robust APIG-based prognostic signature for HCC. CDC25C was a key target through which APs impact HCC and multiple other cancers.

Flow cytometry analysis revealed that Orox A treatment caused G2/M phase arrest in the cell cycle. These findings collectively suggest that Orox A exerts cytotoxic effects on Hep3B cells through mechanisms involving DNA damage, oxidative stress, and cell cycle modulation, making it a promising candidate for further anticancer therapy development.

These findings suggest that SNPs in DNA repair genes, particularly XPC rs2228001, play a crucial role in modulating the prognosis of CCA.

In summary, these data make a strong argument for the notion that Ten/VM-26-mediated inhibition of APEX1 contributes to DNA damage and thereby achieves favorable antilung cancer effects, wherein Ten/VM-26 could down-regulate APEX1 by binding and ubiquitination. The current study presents a critical target and mechanism for Ten/VM-26-mediated antilung cancer therapy.

In this paper, we provide a brief review of the germline and somatic alterations of BER in cancer, with a particular focus on the core enzyme apurinic/ apyrimidinic endonuclease 1 (APE1), encoded by APEX1, and the mechanistic relationship to the development and treatment of cancer. Additionally, the review discusses the latest advances in BER-associated detection technologies and their potential clinical applications, underscoring the therapeutic potential of targeting BER for cancer prevention and intervention.

In the control, a correlation between the transcription levels of genes involved in the functioning of the p53 protein was revealed. An increase in viral load during HPV infection is associated with a change in the coexpression of DNA repair and cell cycle control genes.