IRS2 Promotes Proliferation and Drives Invasion-Migration in SI-NETs.

I investigated the role of insulin receptor substrate 2 (IRS2) in small-intestinal neuroendocrine tumours (SI-NETs). Using SI-NET cell lines (STC-1 and Glu-tag), I found that IRS2 was significantly upregulated. IRS2 knockdown inhibited cellular proliferation, migration, and invasion, while its overexpression promoted these processes. For in vivo validation, I established stable IRS2-knockdown cell lines and performed xenograft experiments in nude mice. Transcriptomic profiling by RNA sequencing was conducted to identify downstream targets of IRS2 signaling. RNA sequencing was performed on control and stable IRS2-knockdown SI-NET cell lines (Glu-tag) in biological triplicate to identify transcriptomic changes induced by IRS2 silencing.

本研究探讨了胰岛素受体底物2（IRS2）在小肠神经内分泌肿瘤（SI-NETs）中的作用。本研究使用小肠神经内分泌肿瘤细胞系（STC-1与Glu-tag）开展实验，发现IRS2的表达显著上调。敲低IRS2可抑制细胞增殖、迁移与侵袭，而过表达IRS2则可促进上述细胞过程。为进行体内验证，本研究构建了稳定敲低IRS2的细胞系，并在裸鼠中开展了异种移植实验。本研究通过RNA测序开展转录组分析，以鉴定IRS2信号通路的下游靶标。此外，本研究对对照组与稳定敲低IRS2的小肠神经内分泌肿瘤细胞系（Glu-tag）进行了三次生物学重复的RNA测序，以鉴定IRS2沉默诱导的转录组变化。