APOBEC1 (Apolipoprotein B MRNA Editing Enzyme Catalytic Subunit 1)

Our study illustrated the characterization of APOBEC mutagenesis in multiple cancer types and highlighted its potential value as a prognostic and immunotherapeutic biomarker for PAAD, and finally demonstrated the effectiveness of irinotecan, an inhibitor of APMs, in vivo and in vitro experiments.

They were also more sensitive to Dasatinib, Bexarotene, and Bicalutamide. APOBEC1 was overexpressed across multiple cancer types and promoted proliferation and migration in LUSC cell lines. This study presents a robust CR-based survival model and highlights APOBEC1 as a potential therapeutic target in LUSC.

Treatment with an UNG inhibitor, adeno-associated virus vector expressing UGI, protected wild-type HSV-1-infected mice from lethal encephalitis. These findings identify uracil-DNA glycosylase as a viral factor enabling evasion from intrinsic antiviral immunity mediated by APOBEC1 in the central nervous system and suggests a potential therapeutic approach to treat HSV-1 encephalitis.

These hypomethylated genes were enriched in drug metabolism pathways, indicating a potential link between genetic ancestry, epigenetic modifications, and pharmacogenomic responses. Combining ancestry, race, and disease type may help identify which patient groups will benefit most from these biomarkers for targeted treatments.

Disruption of the A3 protein association with hnRNPs by A3 mutagenesis diminished A3 mutational activity. This finding not only reveals a regulatory mechanism for A3-induced mutation but also indicates that A3-associated cellular factors can be a potential target for regulating A3-induced mutation for cancer therapeutics.

Gene expression analysis of DNA damage and repair factors revealed that immunotherapy upregulated Apobec1 and Apobec3 genes and downregulated genes related to homologous recombination and translesion synthesis. In conclusion, this study describes the intratumoral immune heterogeneity, that could lead to tumor immune escape, and suggests the potential mechanisms involved.

Here, we provide the first validation of an RNA-SBS mutational signature by decomposing novel exogenous and endogenous APOBEC3A RNA editing signatures into COSMICv3.4 RNA-SBS reference signatures. Additionally, we have identified novel RNA-SBS signatures for APOBEC1, APOBEC3B, and APOBEC3G.

This review clarifies the association between A1CF and other complementary factors and their impact on the development of human diseases, aiming to provide guidance for further research on A1CF, which can help treat human diseases and promote health.

APOBEC/ADAR mutations appeared to potentiate the impact of DRR defects on several mutational signatures, and some factors seemed to inversely affect certain signatures. These findings potentially implicate certain APOBEC/ADAR mutations/mRNA levels in distinct mutational signatures, particularly APOBEC1 mRNA levels in aging-related signatures and ADARB1 mRNA levels in UV radiation-related signatures.

Notably, primary and metastatic samples from renal cancer patients exhibited high A1CF expression, low p65(Ser536) phosphorylation, and decreased IFN-β levels in renal carcinoma tissues compared with the corresponding paracancerous tissues. Our results indicate that A1CF-decreased p65(Ser536) phosphorylation and IFN-β levels may be caused by A1CF competitive binding to the p65-combined site on NKRF and demonstrate the direct binding of A1CF independent of RNA or DNA in signal pathway regulation and tumor promotion in renal carcinoma cells.

TINAG, DDC, SPDEF, and APOBEC1 could serve as new PAAD predictors. The risk model developed in this study could be used to predict the prognosis of PAAD patients.