S100A16 (S100 Calcium Binding Protein A16)

Clinical validation revealed that high S100A16+ TECs abundance correlated with vascular invasion, immunotherapy resistance, and shorter progression-free survival. Our study identifies S100A16+ TECs as a distinct endothelial subpopulation that drives HCC progression through coordinated promotion of pathological angiogenesis and immunosuppression, representing a potential therapeutic target and biomarker for immunotherapy response prediction in HCC.

Kyoto Encyclopedia of Genes and Genomes analysis revealed pathways related to morphine addiction and protein digestion/absorption...Sensitivity to chemotherapeutics, such as AZD6482, ABT-263, A-770041, and BMS-536924, was observed in LUAD. Reverse transcription-quantitative polymerase chain reaction validation results demonstrated that KRT8 and S100A16 were significantly upregulated in tumor tissues, while COL4A3 and SMAD9 expression was downregulated, which was consistent with the TCGA-LUAD database analysis. In conclusion, 6 genes (KRT8, S100A16, COL4A3, SMAD9, MAP3K8, and CCDC146) were identified as potential biomarkers, offering valuable insights into LUAD pathogenesis and therapeutic strategies.

In conclusion, our research revealed that S100A16 silencing downregulated RPN2 levels through p-STAT3, thereby inhibiting the p-GSK3β/β-catenin/TCF signaling pathway. These findings highlight S100A16 as a potential therapeutic target for cervical cancer.

Clinically, elevated S100A16 expression correlated with enrichment of ribosome biogenesis pathways and reduced relapse-free survival in metastatic breast cancer patients. In summary, we identified a critical role for S100A16 as a molecular modulator in the nucleolus that impinges upon breast cancer metastasis.

We also found that overexpression of ANXA2 can restore the decreased levels of p-PI3K and p-AKT induced by S100A16 inhibition, which indicated that S100A16 stimulates PI3K/AKT pathway activation via ANXA2. To sum up, S100A16 can promotes osteosarcoma progression by activating the PI3K/AKT signaling pathway through ANXA2, suggesting that the S100A16/ANXA2 axis may represent a novel therapeutic target for osteosarcoma.

QRT-PCR detection of Clinical LUAD samples also validated the differentially expression of CDIGPM model related genes.ConclusionsThe study highlights the prognostic importance of CDIGs in LUAD using the CDIGPM model, linking age, stage and CDIGPM score to poor outcomes. The identified genes and pathways provide potential therapeutic targets, deepening our understanding of LUAD's molecular landscape.

In conclusion, this study establishes MRMS as a robust prognostic biomarker and highlights its dual role in shaping the tumor immune microenvironment and guiding therapeutic strategies. These findings provide novel insights into mitochondrial RNA modifications and their potential applications in personalized treatment for LUAD.

Novel collections of miRNAs, such as has-miR-423-5p, has-miR-769-5p, has-miR-151a-3p, and has-miR-550a-5p, targeting S100A16 at a pan-cancer level were predicted through various databases. These findings contribute to a comprehensive understanding the role of S100A16 in prognosis prediction, chemotherapy, and immunotherapy, providing valuable insights for identifying novel targets in cancer treatment.

Furthermore, the interaction between MOV10 and integrin α3 (ITGA3) was verified by RNA immunoprecipitation assay, and the actinomycin D assay was used to detect ITGA3 mRNA stability...Furthermore, it was demonstrated that S100A16 regulated the stability of ITGA3 mRNA via MOV10 to mediate ECM‑receptor interactions. In conclusion, S100A16 may bind to MOV10 to stabilize ITGA3 mRNA and regulate ECM‑receptor interactions, hence contributing to the malignant progression of LUAD.

The research established a prognostic model consisting of 16 genes, and a nomogram was developed to accurately predict the prognosis of LUAD patients. These findings may contribute to guiding clinical decision-making and treatment selection for patients with LUAD, ultimately leading to improved treatment outcomes.

Key gene S100A16 in the CPM model was validated as an oncogene, enhancing LUAD cell proliferation, invasion and migration. The CPM model emerges as a novel biomarker for predicting prognosis and immunotherapy response in LUAD patients, with S100A16 identified as a potential therapeutic target.

Furthermore, our findings suggested that S100A16 acted as an oncogenic factor to promote aggressiveness and GEM resistance in PC cells. In conclusion, the current findings provide new mechanistic insights into PC aggressiveness and GEM resistance, suggesting the critical role of circ_0036627/miR-145/S100A16 axis in PC progression and drug resistance development and offering novel therapeutic targets for PC therapy.