DUSP9 (Dual Specificity Phosphatase 9)

Oncofetal reprogramming-based prognostic signature robustly stratifies HCC patient survival across independent cohorts. DUSP9 is identified as a core oncofetal regulator that drives stem-like traits in HCC. Mechanistically, DUSP9 suppresses ERK1/2-phosphorylation, stabilizes PPARG, and transcriptionally activates SCD. The DUSP9-ERK1/2-PPARG-SCD axis remodels lipid metabolism to support proliferation, cell mobility, and sorafenib resistance.

Furthermore, DUSP9 expression in tumor tissues exhibited an inverse relationship with immune cell infiltration within the tumor microenvironment (TME). In conclusion, this study provided evidence that DUSP9 was up-regulated in HNSCC tissues and may play a pivotal role in HNSCC progression, suggesting its potential as a novel biomarker.

The GIS system is an effective biomarker for evaluating GI, prognosis, and immune features in HNSCC. The findings also clarify the functional mechanism of the GI-related ceRNA axis RNF216P1/let-7b-5p/DUSP9, providing valuable insights for future research and the development of therapeutic strategies for HNSCC.

Canine HCC may involve different angiogenesis mechanisms. CT findings can be used to assess the gene expression status in canine HCC and may add new value to CT imaging.

In summary, we explored the dysregulated transcriptome profile that IGF2BP3 affects gene expression and alternative splicing by binding to mRNA, and thus plays a role in the development of GC cells. The IGF2BP3 and identified targets has potential value for GC treatment in future.

This study systematically explored the TLS and related genes from the perspectives of bioinformatics, clinical features and cytology experiments. The total-gene TLS score, risk score and TNFSF14 hub gene may be useful biomarkers for predicting the prognosis and immunotherapy efficacy of soft tissue sarcoma.