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Abstract：
BACKGROUND: The mechanisms by which SLC2A1 enhances chemo-resistance of taxanes to non-small cell lung cancer (NSCLC) remains enigmatic.
METHODS: An investigation into the SLC2A1 expression pattern and prognosis across diverse datasets, as well as our internally collected samples, was undertaken. Additionally, the biological function of SLC2A1 was further delved into through in vitro experiments. The study also examined the chemo-resistance of NSCLC to taxanes using CCK-8, Annexin-V, and caspase-3 assays. Furthermore, the impact of taxanes on SLC2A1 expression was determined via western blot analysis. The effects of SLC2A1 on the formation of CSCs was examined via flow cytometry and metabolomics techniques. Finally, the impact of SLC2A1 on the tumor microenvironment was analyzed using single-cell sequencing and cellchat.
RESULTS: In the present investigation, it was observed that there was an elevated expression of SLC2A1 in NSCLC tumor tissues, which exhibited a significant association with a poorer prognosis. SLC2A1 overexpression in vitro promoted NSCLC cell proliferation, invasion, migration, chemo-resistance, and the formation of CD90+ and EpCAM+ CSCs. NSCLC cells were categorized based on SLC2A1 and EpCAM expression. SLC2A1highEpCAM+ CSCs were more chemo-resistance to taxanes. NSCLC patients with high SLC2A1 and EpCAM expression had poorer prognosis. Mechanically, SLC2A1 promoted the formation of CD90+ and EpCAM+ CSCs via activating glycolysis. Finally, SLC2A1low tumor cells promoted CD8+T cell function via HLA-A, B, C, and suppressed NK cell function via HLA-E.
CONCLUSIONS: Together, SLC2A1 plays an important role in enhancing chemo-resistance of taxanes to NSCLC.
METHODS: An investigation into the SLC2A1 expression pattern and prognosis across diverse datasets, as well as our internally collected samples, was undertaken. Additionally, the biological function of SLC2A1 was further delved into through in vitro experiments. The study also examined the chemo-resistance of NSCLC to taxanes using CCK-8, Annexin-V, and caspase-3 assays. Furthermore, the impact of taxanes on SLC2A1 expression was determined via western blot analysis. The effects of SLC2A1 on the formation of CSCs was examined via flow cytometry and metabolomics techniques. Finally, the impact of SLC2A1 on the tumor microenvironment was analyzed using single-cell sequencing and cellchat.
RESULTS: In the present investigation, it was observed that there was an elevated expression of SLC2A1 in NSCLC tumor tissues, which exhibited a significant association with a poorer prognosis. SLC2A1 overexpression in vitro promoted NSCLC cell proliferation, invasion, migration, chemo-resistance, and the formation of CD90+ and EpCAM+ CSCs. NSCLC cells were categorized based on SLC2A1 and EpCAM expression. SLC2A1highEpCAM+ CSCs were more chemo-resistance to taxanes. NSCLC patients with high SLC2A1 and EpCAM expression had poorer prognosis. Mechanically, SLC2A1 promoted the formation of CD90+ and EpCAM+ CSCs via activating glycolysis. Finally, SLC2A1low tumor cells promoted CD8+T cell function via HLA-A, B, C, and suppressed NK cell function via HLA-E.
CONCLUSIONS: Together, SLC2A1 plays an important role in enhancing chemo-resistance of taxanes to NSCLC.
摘要：
背景：SLC2A1增强紫杉烷类对非小细胞肺癌（NSCLC）的化学抗性的机制仍然是一个谜。
方法：对不同数据集的SLC2A1表达模式和预后进行调查，以及我们内部收集的样本，进行了。此外,通过体外实验进一步研究了SLC2A1的生物学功能。该研究还使用CCK-8，膜联蛋白-V检查了NSCLC对紫杉烷的化学抗性，和caspase-3测定。此外，紫杉烷类对SLC2A1表达的影响通过蛋白质印迹分析确定.通过流式细胞术和代谢组学技术检查SLC2A1对CSC形成的影响。最后,使用单细胞测序和细胞聊天分析了SLC2A1对肿瘤微环境的影响.
结果：在本调查中，观察到SLC2A1在NSCLC肿瘤组织中的表达升高，表现出与预后较差的显着关联。SLC2A1过表达促进NSCLC细胞增殖,入侵,迁移,化学抗性，CD90+和EpCAM+CSCs的形成。基于SLC2A1和EpCAM表达对NSCLC细胞进行分类。SLC2A1highEpCAM+CSC对紫杉烷类具有更高的化学抗性。SLC2A1和EpCAM高表达的NSCLC患者预后较差。机械上,SLC2A1通过激活糖酵解促进CD90+和EpCAM+CSC的形成。最后,SLC2A1低肿瘤细胞通过HLA-A促进CD8+T细胞功能，B,C,通过HLA-E抑制NK细胞功能
结论：一起，SLC2A1在增强紫杉烷类对NSCLC的化学抗性中起重要作用。
方法：对不同数据集的SLC2A1表达模式和预后进行调查，以及我们内部收集的样本，进行了。此外,通过体外实验进一步研究了SLC2A1的生物学功能。该研究还使用CCK-8，膜联蛋白-V检查了NSCLC对紫杉烷的化学抗性，和caspase-3测定。此外，紫杉烷类对SLC2A1表达的影响通过蛋白质印迹分析确定.通过流式细胞术和代谢组学技术检查SLC2A1对CSC形成的影响。最后,使用单细胞测序和细胞聊天分析了SLC2A1对肿瘤微环境的影响.
结果：在本调查中，观察到SLC2A1在NSCLC肿瘤组织中的表达升高，表现出与预后较差的显着关联。SLC2A1过表达促进NSCLC细胞增殖,入侵,迁移,化学抗性，CD90+和EpCAM+CSCs的形成。基于SLC2A1和EpCAM表达对NSCLC细胞进行分类。SLC2A1highEpCAM+CSC对紫杉烷类具有更高的化学抗性。SLC2A1和EpCAM高表达的NSCLC患者预后较差。机械上,SLC2A1通过激活糖酵解促进CD90+和EpCAM+CSC的形成。最后,SLC2A1低肿瘤细胞通过HLA-A促进CD8+T细胞功能，B,C,通过HLA-E抑制NK细胞功能
结论：一起，SLC2A1在增强紫杉烷类对NSCLC的化学抗性中起重要作用。
