GALNT2 (Polypeptide N-Acetylgalactosaminyltransferase 2)

The study also identified six key genes, among which both the silencing and overexpression of GALNT2 significantly affect the proliferation and migration of melanoma cells. This study highlights the significance of MRGs in predicting patient survival and immunotherapy outcomes, providing insights for potential future targeted therapies.

GEPIA research and microarray data revealed that FUT2 expression was higher in colorectal cancer tissues than in normal tissues and that individuals with colon cancer with high expression of FUT2 had longer overall survival times. Our study highlights the significant impact of genetic variants on glycosylation pathways and offers novel insights into potential biomarkers for colorectal cancer risk.

Notably, we observed that GALNT1 and GALNT2 modulated EGFR protein expression. Overall, our findings suggest that the combined activity of GALNT1 and GALNT2 is critical in regulating HCC malignant behaviors.

Using a reporter gene mouse line, we demonstrated that adipocytes originate through transdifferentiation from pancreatic cells. GalNT2 overexpression results in additional O-glycosylation sites, which we analyzed through PNA lectin enrichment and mass spectrometric proteome analysis.

We identified potential therapeutic drugs, including the MEK inhibitor (PD-184352)...We identified a distinct LUAD GT gene signature, and these differentially expressed mRNAs could serve as valuable prognostic biomarkers and therapeutic targets. Furthermore, we experimentally validated their expression levels and identified potential therapeutic agents.

The creation of a LUAD single-cell atlas in our study offered new insights into its tumor microenvironment and immune cell interactions, highlighting the importance of key genes associated with exhausted CD8+ T cells. These discoveries have enabled the development of an effective prognostic model for LUAD and identified GALNT2 as a potential therapeutic target, significantly contributing to the improvement of LUAD diagnosis and treatment strategies.

Based on our experiments, miR-139-5p overexpression inhibited RCC proliferation, and this phenotype was rescued by GALNT2 overexpression. Given these evidences, the miR-139-5p-GALNT2-LATS2 axis is critical for RCC proliferation, and it is an excellent candidate for a new therapeutic target in ccRCC.

Sarcopenia may be related to immunosuppressive microenvironment and affect the prognosis of AML patients.

These findings indicate that circ-hnRNPU inhibits NONO-mediated c-Myc transactivation and mRNA stabilization essential for glycosylation and cancer progression.

In summary, our findings established GALNT2 as a key contributor to the radioresistance of NSCLC. Therefore, targeting GALNT2 may be a promising therapeutic strategy for NSCLC.

The classifier we constructed may help improve our understanding of subtype characteristics and provide a new strategy for developing CESC therapeutics. Remarkably, GALNT2 may be an option to directly target drivers in CESC cancer therapy.

Through a rational screening, we found a GALNT2 inhibitor that dramatically suppresses GSCs self-maintenance in vitro and in vivo. Collectively, we uncovered the critical function of GALNT2 in promoting GSCs self-maintenance and GBM progression and may provide a new potential drug for GBM clinical therapy.