PABPC1L (Poly(A) Binding Protein Cytoplasmic 1 Like)

The combined four-gene model demonstrated moderate discriminatory power, yielding an AUC of 0.76 (95 % CI 0.65-0.86, p < 0.0001) with balanced sensitivity and specificity of 69.8 % each at the 0.5 cutoff (overall accuracy 69.8 %). Taken together, RUSC1-AS1, SNHG17, PABPC1L and SNHG1 can be novel candidates for future diagnostic studies in CRC.

This study successfully identified and developed a prognostic signature based on nine RBPs, accompanied by a nomogram for predicting survival probability in BLCA patients. Our findings demonstrate that these nine RBPs function as significant biomarkers for forecasting the prognosis and immune status in BLCA, suggesting their potential as therapeutic targets for BLCA.

We developed a risk signature constructed based on the five LLPS-related genes and can have a high ability to predict the prognosis of ccRCC patients, further providing a strong support for clinical decision-making.

Conversely, loss of PABPC1L diminished IDO1 expression, mitigated cytotoxic T-cell suppression, and enhanced responsiveness to anti-PD-1 therapy in patient-derived xenograft models. These findings reveal the crucial role of PABPC1L in facilitating immune evasion in RCC and indicate that inhibiting PABPC1L could be a potential immunotherapeutic approach in combination with ICB to improve patient outcomes.

Enrichment analysis showed that biological functions, such as cadherin binding, Golgi vesicle transport, protein folding, and cell adhesion molecules were related to GS progression. In conclusion, this study provides insight into ST-based transcriptome-wide expression patterns during GS progression.

Low risk patients were more sensitive to small molecule drugs including Erlotinib, Sunitinib, MG-132, CGP-082996, AZ628, Sorafenib, VX-680, and Z-LLNle-CHO. Four risk genes (CALB1, CPA3, NOXA1, and TNNT1) had significant positive correlation with their methylation level, while six genes (CCL22, GPRC5B, HSPA1A, MFNG, PABPC1L, and PCOLCE2) were negatively correlated with their methylation level. This study provides novel understanding of heterogeneity in COAD from the perspective of senescence, and develops signatures for prognosis prediction in COAD.