Niclosamide Suppresses Gastric Cancer Progression through YTHDF2 Inhibition-Affected Lactate Metabolic Reprogramming
Description
This study hypothesizes that the anti-tumor effects of niclosamide in gastric cancer (GC) are mediated through the disruption of metabolic reprogramming, specifically by targeting the m6A reader protein YTHDF2, which in turn influences the expression of key metabolic genes. This dataset contains original experimental data that validates the role of YTHDF2 and the mechanism of niclosamide action. The Western Blot (immunoblot) data demonstrates the protein-level expression of YTHDF2 and its downstream metabolic target genes upon niclosamide treatment. Immunohistochemistry (IHC) images Visualize the in situ expression and spatial localization of YTHDF2 and metabolic pathway components within gastric cancer tissue, providing pathological context. Transwell assay images quantitatively documenting the inhibitory effect of niclosamide on GC cell migration and invasion capabilities. Colony formation assay images directly showing the suppressive impact of niclosamide on GC cell proliferation and long-term clonogenic survival.