B3GNT3 (UDP-GlcNAc:BetaGal Beta-1,3-N-Acetylglucosaminyltransferase 3)

Collectively, TCN1 overexpression aggravated NSCLC progression by regulating the expression of B3GNT3. The TCN1-B3GNT3 axis served a key part in the growth, migration, invasion, and glycolysis of NSCLC cells, making it a potential therapeutic target for NSCLC treatment.

High CANT1 and B3GNT3 expressions are associated with aggressive clinicopathological features in IDC and predict unfavourable outcomes. These markers may serve as potential prognostic indicators and independent predictors of LNM in IDC patients.

RNA sequencing analysis identified significantly upregulated genes in Gemcitabine (Gem)-resistant cells of PDAC(ASPC-1/Gem)...Mechanistically, FUT3 bound to β-1,3-N-acetylglucosaminyltransferase 3 (B3GNT3) to activate Nuclear Factor-kappa B (NF-κB) signal transduction, driving autophagy, progression and chemoresistance. Our results reveal that FUT3 interacts with B3GNT3 and activates the NF-κB signaling, amplifying autophagic activity to drive PDAC progression and confer chemoresistance.

Based on these genes, we also identified several potential therapeutic agents and conducted drug sensitivity analyses. This study elucidated the potential mechanisms of NECSO in LUAD and established an effective prognostic model, offering novel insights for the diagnosis and treatment of LUAD.

Immunohistochemical validation confirmed that B3GNT3 is highly expressed in real-world cases of PAAD, COAD, LUAD, UCEC, and OV. Pan-cancer analysis of B3GNT3 reveals complex regulatory mechanisms across different types of cancer, emerging as a novel biomarker for cancer diagnosis and prognosis, and offers new avenues for targeted therapeutic development.

These three CDDP resistance-associated lncRNAs including ARAP1-AS2, LINC01843, and LINC02198, serve as reliable prognostic biomarkers for LUAD. The findings provide insights for immunotherapeutic strategies and personalized treatment development.

qRT-PCR confirmed that, except for NLRP10, all prognostic genes exhibited expression patterns consistent with TCGA-NSCLC data. This study highlights the significant role of FRGs in NSCLC prognosis and regulation, offering novel insights for personalized treatment strategies.

They are consistent with the important roles of the associated pathways in LUAD oncogenesis induced by smoking, including estrogen response, apical junction and glycolysis pathways. In summary, our study may provide valuable insights into exploring ATAC-seq peaks and understanding smoking-related LUAD carcinogenesis from a perspective of open chromatin changes.

The results of this study underscore the importance of sex differences in cancer biology and indicate that this methodology, BioOptimatics, can help in the discovery of new pathways and biomarkers for BC and CRC in women.

Thus, in the follow-up study, we will demonstrate the functional role of FXYD3 in pancreatic cancer tumorigenesis. This study revealed that the FXYD3 may act as a significant oncogene in the early stage of pancreatic cancer.

Conclusion  RNA sequencing is a viable and informative approach for genomic profiling of archival SNUC samples. Both SR-SNUC and SD-SNUC were noted to have distinct genetic profiles underlying the molecular classification of these diseases.

Bioinformatics analysis indicated that B3GNT3 may play a role in immune regulation by regulating M2 macrophages. This study developed a new prognostic model for ESCC and identified B3GNT3 as a potential biomarker negatively associated with lymph node metastasis, which warrants further validation.