FXYD3 (FXYD Domain Containing Ion Transport Regulator 3)

Using a novel data-driven approach, six potential imaging targets were successfully identified and validated. CEACAM5 and CEACAM6 emerged as strong targets that, regardless of neoadjuvant therapy, covered nearly the entire CRLM population-supporting their further probe development and clinical translation.

The targeted FXYD3 nano-delivery system (siFXYD3@PEP) exhibited significant antitumor efficacy in spontaneous and transplanted tumor models and markedly enhanced the sensitivity of ICC to standard gemcitabine and cisplatin chemotherapy. Our findings highlight the role of FXYD3 in cancer-related inflammation and innate immune signaling, thereby providing a new paradigm for understanding the pathogenesis of ICC.

Additionally, the levels of the phosphorylated forms of FAK, AKT, and mTOR were significantly reduced in both AGS/DDP and SGC-7901/DDP cells treated with the combination of DDP and SSD, whereas the PTEN expression level increased. Our findings highlight the importance of alternative components within the tumor microenvironment for GC therapy and identify FAK/AKT/mTOR signaling as a potential target of SSD, providing novel insights into the mechanism by which SSD improves DDP resistance in GC.

Drug sensitivity analysis showed high-risk groups were resistant to Cisplatin (P = 0.003), Mitomycin C (P = 0.01), and Paclitaxel (P = 0.004), with IC50 values significantly higher than low-risk groups. Its integration with clinical features enhances personalized treatment strategies, highlighting the importance of ICD in BLCA immunotherapy and precision medicine. The model's predictive accuracy and biological relevance were validated across multiple datasets, underscoring its potential for clinical application.

Furthermore, drug sensitivity analysis revealed that the MaGPS signature scores were significantly associated with the sensitivity to 38 different drugs, highlighting potential targeted therapies related to MaGPS. The MaGPS model, based on bulk RNA-seq, scRNA-seq, and spatial transcriptomics data, effectively evaluated the prognosis of pancreatic cancer and provided valuable insights for better therapeutic targets.

Immunohistochemical FXYD3 expression does not predict survival in chemo-naive PDAC patients, but is associated with late-stage disease. The high rate of FXYD3 overexpression warrants therapeutic evaluation.

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.

The five drugs, including topotecan, PD-0325901, panobinostat, paclitaxel and 17-AAG, with the highest activity among 27 PDAC cell lines were filtered. Overall, the diagnostic model built based on four significant DMRs could accurately distinguish tumor and normal tissues. The five drug candidates might be repurposed as promising therapeutics for particular PDAC patients.

The expression patterns of miR-8114, Myl4, Col1a1, Tmem163, Myl7, Sln, and Fxyd3, which belong to the top 30 DEGs, were verified by quantitative real-time PCR (RT-qPCR). In summary, this study firstly discloses novel insights into the regulatory mechanisms underlying PC6-based EA therapy against CFZ-induced cardiotoxicity, potentially serving as a theoretical foundation for further clinical applications.

Our results demonstrate aberrant expression patterns, prognostic values, and oncogenic activities of FXYD genes in OCa. FXYD1, FXYD5 and FXYD7 may serve as biomarkers and therapeutic targets for this disease. Targeting FXYD-mediated signaling represents a promising therapeutic strategy against OCa.

Together, our data indicate that FXYD3+ CSCs with ancestral features are drivers of plasticity and chemoresistance in TNBC. Targeting the Na+/K+ pump could be an effective strategy to eliminate CSCs with ancestral and DTP features that could improve TNBC prognosis.

Prediction of clinical progression remains elusive in PCa. This research uncovers novel splicing events associated with BCRFS, augmenting existing prognostic tools, thus potentially refining clinical decision-making.