Niclosamide Suppresses Gastric Cancer Progression through YTHDF2 Inhibition-Affected Lactate Metabolic Reprogramming

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.本研究提出如下假说：氯硝柳胺（niclosamide）在胃癌（gastric cancer，缩写GC）中的抗肿瘤作用，通过干扰代谢重编程（metabolic reprogramming）介导，具体机制为靶向m6A阅读蛋白（m6A reader protein）YTHDF2，进而调控关键代谢基因的表达。 本数据集包含验证YTHDF2作用及氯硝柳胺作用机制的原始实验数据：其中，蛋白质免疫印迹（Western Blot，immunoblot）数据展示了经氯硝柳胺处理后，YTHDF2及其下游代谢靶基因的蛋白水平表达情况；免疫组织化学（Immunohistochemistry，缩写IHC）图像可呈现胃癌组织内YTHDF2及代谢通路组分的原位表达与空间定位，为研究提供病理学背景；Transwell实验图像定量记录了氯硝柳胺对胃癌细胞迁移与侵袭能力的抑制效果；集落形成实验图像则直接展现了氯硝柳胺对胃癌细胞增殖及长期克隆存活的抑制作用。