CBR3 (Carbonyl Reductase 3)

HSDL2, AMACR, and CBR3 were established as prognostic biomarkers for CC. The risk model demonstrated robust predictive accuracy, offering a scientific foundation for clinical prognosis prediction in CC.

For CBR3 (rs8133052), the GA genotype was significantly associated with a higher risk of anemia (OR 3.5; 95% CI: 1.05-11.7; p = 0.042), acute cardiotoxicity (OR 4.4; 95% CI: 1.86-11.5; p = 0.002), cardiac-related symptoms, and higher peak plasma DOX levels, along with reduced complete response. Polymorphisms in ABCC2 and CBR3 genes may contribute to individual variability in DOX-related toxicity and treatment response.

The integrated model combining 5-lncRNA molecular signature with clinical parameters demonstrates significant prognostic stratification capacity and therapeutic decision-making value in EBC management. It may help patients consult and personalize disease management.

Anthracyclines (doxorubicin, epirubicin, daunorubicin, idarubicin) are among the most used drugs for the treatment of breast cancer. Even though, NCF4 rs1883112 showed a risk reduction tendency, suggesting the potential for personalized risk stratification. We can conclude that multiple genes are involved in ABCC, with different impacts, and it is unlikely that there is a single driver gene in ABCC pathogenesis.

In GC, CBR3-AS1 and PCA3 may be utilized as therapeutic targets and prognostic biomarkers, respectively.

Detecting CBR3 genetic polymorphisms is crucial for assessing cardiotoxicity before administering DOX, and monitoring BNP levels helps early detection. CBR3 is also associated with DOX anemia.

Our findings suggested that polymorphisms in CBR1, CBR3, AKR1C3, ABCB1, and ABCG2 were unlikely to be reliable predictors of cumulative plasma exposure to DOX and DOXol. Therefore, mitigating the risk of cumulative plasma exposure to DOX and DOXol through PK approaches may require the development of novel therapeutic drug monitoring strategies. Supplementary file1 (MP4 3804 KB).

Our study identifies methyltransferase RBM15 as a potential therapeutic target for NSCLC radioresistance whose inhibition reverses resistance through limiting MDSC recruitment via the m6A-IGF2BP3-CBR3-AS1/miR-409-3p/CXCL1 axis.

In summary, there were differences in genomic alterations, somatic interactions and the serum levels of Cr between patients with NSCLC with hypertension and patients with NSCLC without hypertension. Furthermore, patients with hypertension exhibited significant negative correlations between Cr and CEA, between CYFRA21-1 and Zn, and between NSE and As, suggesting that heavy metals may contribute to the occurrence of NSCLC with different hypertensive status.

Upregulated expression of lncRNA CBR3-AS1 showed significant association with unfavorable survival and indicated worse clinicopathological outcomes in multiple kinds of human cancer, and therefore might serve as a promising prognosis biomarker and therapeutic target for cancers.

Among these, IGF2R (OR = 1.165; 95% CI 1.067-1.272; p = 1.046 × 10- 2) and CST3 (OR = 0.523; 95% CI 0.339-0.804; p = 7.010 × 10- 3) were highlighted as key drug targets with causal evidence both at transcriptional and translational levels. This study preliminarily confirms that IGF2R and CST3 may serve as novel targets for the treatment of EC, providing a foundational reference for innovative clinical approaches to this disease.

Further bioinformatics analysis showed that the major interacted genes of KCNA6 were enriched in several resistance-associated pathways including interleukin -17 signaling pathway and cyclic adenosine monophosphate signaling pathway. In conclusion, this work indicates that CBR3-AS1 might be involved in BCR::ABL1 independent TKI resistance of CML patients through targeting KCNA6, providing a novel target for intervention treatment of CML patients with BCR::ABL1 independent TKI resistance.