EGLN3 (Egl-9 Family Hypoxia Inducible Factor 3)

In an external validation cohort, an area under the curve (AUC) of 0.922 for low-grade ccRCC detection and 0.874 for high-grade ccRCC detection was achieved, respectively, using urinary EVs. Furthermore, integrating single-cell sequencing data revealed that SERPINA1 and VEGFA in low-grade ccRCC, and APOC1 and TGFBI in high-grade ccRCC, were derived from tumour-associated macrophages, whereas NDUFA4L2 originated from cancer cells in both low- and high-grade ccRCC.

Modulating this metabolic shift, either by supplementing exogenous lysophospholipids or depleting Egln3 in AML cells, restored the phospholipid balance and mitigated the protumorigenic effects induced by CD81+ Erys. Overall, our findings elucidate the molecular crosstalk between erythroblasts and AML cells, extend our insights into the mechanisms driving AML progression, and suggest potential therapeutic strategies.

This study provides new insights into EGLN biology and identifies EGLN1 as a potential biomarker for cervical cancer.

This study provides novel insights into the transcriptional landscapes in TNBC BM using spRNA-seq, emphasizing the role of neuron-tumor interactions and immune dynamics. These findings suggest new therapeutic strategies and underscore the importance of further research.

HOXC9 is overexpressed in HCC and correlates with poor prognosis. The HRIG-based risk score model effectively evaluates the prognosis and immune response in HCC patients, providing new insights for risk assessment and immunotherapy prediction.

Finally, the experimental findings indicated that Troxerutin exhibits a strong binding energy to the sialylation-related gene EGLN3, which could greatly reduce the growth of LUAD by inhibiting the expression of EGLN3, thus limiting the capacity of LUAD cells in the proliferation, migration, and invasion. Troxerutin could target and lower the expression of sialylation-related gene EGLN3, reducing LUAD cells' ability to proliferate, migrate, and invade, making it an essential reference for LUAD prevention and treatment.

In vitro and in vivo assays both confirmed that the FOXD2-AS1/MYC/EGLN3 axis could accelerate the progression of ccRCC. FOXD2-AS1 activated EGLN3 to accelerate ccRCC cell functions via binding to the transcription factor MYC.

JTGs can improve the degeneration of joint cartilage and achieve the purpose of cartilage protection, which can be used for the treatment of OA. SMSCs-related miRNA expression profiles were significantly altered after the intervention with JTGs containing serum. The 9 co-differentially expressed genes may be the key targets for the efficacy of JTGs in the treatment of OA rats, which can be used for subsequent validation.

We comprehensively investigated the expression pattern, single-cell function, immune infiltration level and regulated signaling pathway of EGLN3 in pan-cancer. We found that EGLN3 is an important hypoxia and immune-related gene that may serve as a potential target for tumor immunotherapy.

Moreover, MTCs with desmoplasia had a significantly increased expression of DLL3. Our data supports the idea that DLL3 should be further explored as a predictor of aggressive disease and poor outcomes in MTC.

In conclusion, the differential expression of EGLN and HIF1A genes in HNSCC tumors compared to normal tissues influences patients' overall survival, highlighting their role in tumor development. Moreover, DNA methylation could be responsible for HIF1A suppression in the normal tissues of HNSCC patients.

Additionally, DPA was found to significantly induce EGLN 3 expression in CRC cell lines. These results suggest that FAA modulate gut microbial composition, enhance protective metabolites, improve gut barrier functions, and inhibit carcinogenic pathways.