SLC5A1 (Solute Carrier Family 5 Member 1)

Metformin pretreatment significantly enhanced PBMC-mediated cytotoxicity against tumor cells and patient-derived organoids in ex vivo co-culture systems. Our findings establish the SLC5A11-AMPK-PD-L1 axis as a novel mechanism linking metformin to tumor immunity, providing a molecular rationale for combining metformin with checkpoint inhibitors in cancer immunotherapy.

This study comprehensively characterized the molecular features of ArMGs in GC and developed a robust, validated prognostic prediction model. The findings offer new molecular insights for predicting patient outcomes and guiding personalized therapeutic strategies in GC.

The qRT-PCR results showed that C2CD4A, CERS1, MMP9, SLC5A1, HORMAD2 were highly expressed in the IHH4, KTC-1, and TPC-1 cell lines, while SLITRK2, ARHGEF37, PLP1, RNF223, and F3 were lowly expressed. The TBSMRPM established in this study has a certain value for the prognosis of thyroid cancer and contributes to refine clinicians' treatment protocols.

The negative effects limit the application of FMT/FVT. Identifying the primary functional components of FMT/FVT to develop safe and targeted microbial preparations is one potential solution.

Furthermore, inhibiting lactate uptake by lactate transporters, specifically by SLC5A12 blockade, represents a previously unappreciated checkpoint in autoimmune inflammatory diseases. This approach results in multidimensional pro-resolution effects, including reduced inflammatory cytokine levels, enhanced T cell egress from inflamed sites and diminished T cell and B cell areas and their segregation within ELS.

We hypothesize that SGLT-1 might play a role in the plasticity of pancreatic β-cells and suggest mechanisms through which CGGM patients could potentially have a higher risk of developing insulinoma in adulthood. This is the first documented case of insulinoma in a patient with CGGM, suggesting a potential new link between glucose absorption disorders and pancreatic neuroendocrine tumors.The loss-of-function mutation in SGLT-1 due to an SLC5A1 gene mutation may impact pancreatic β-cell plasticity, potentially contributing to insulinoma development through altered glucose homeostasis.The patient's long-term high-fat, low-carbohydrate diet may have played a role in β-cell stimulation via increased levels of GLP-1 and GIP, both of which promote β-cell proliferation and survival.

This study is the first to identify ALV-J resistance-associated genetic markers in Chengkou mountain chickens, revealing key genes related to immune regulation, membrane function, and tumor development. The findings provide a foundational molecular basis for disease-resistant breeding in poultry.

This study identifies PLOD2 as a key prognostic biomarker and therapeutic target in gastric cancer. As a central component in a glycometabolism-related model, PLOD2 promotes glycolysis, tumor progression, and immune evasion via the PI3K/AKT/mTOR pathway. The model effectively stratifies patient risk, offering both prognostic utility and therapeutic insight. Targeting PLOD2-mediated pathways may represent a promising strategy for precision therapy and improved clinical outcomes in gastric cancer.

P=N/A, N=140, Recruiting, Johns Hopkins University

Additionally, inhibiting SLC5A1 and CACNB2 showed a connection to lower OPC risk. These findings suggest that targeting these genes could offer promising therapeutic strategies for preventing and treating HNC, as well as improving both preoperative and postoperative management in affected patients.

Overexpressing SLC5A1 significantly reduced the inhibitory effects of Hesperidin, highlighting its crucial role in this context. Hesperidin exerts its anticancer effects on colon cancer by inhibiting SLC5A1 expression and consequently downregulating EGFR phosphorylation.

Drug sensitivity analysis suggested that Metformin, Gefitinib, and Lapatinib may be more effective in the low-risk group, while Pyrimethamine, Axitinib, and Rapamycin may be more beneficial for high-risk patients. In summary, we identified a 6-gene signature related to dendritic cell dysfunction that can predict prognosis in esophageal cancer, offering valuable insights for personalized therapeutic strategies.