Institute of Physiology, University of Zurich, 8057, Zurich, Switzerland.
Department of Pathology and Molecular Pathology, University Hospital Zurich, 8091, Zurich, Switzerland.
Nat Commun. 2017 Nov 13;8(1):1466. doi: 10.1038/s41467-017-01514-3.
Renal angiomyolipomas (AML) contain an admixture of clonal tumour cells with features of several different mesenchymal lineages, implying the existence of an unidentified AML neoplastic stem cell. Biallelic inactivation of TSC2 or TSC1 is believed to represent the driving event in these tumours. Here we show that TSC2 knockdown transforms senescence-resistant cultured mouse and human renal epithelial cells into neoplastic stem cells that serially propagate renal AML-like tumours in mice. mTOR inhibitory therapy of mouse AML allografts mimics the clinical responses of human renal AMLs. Deletion of Tsc1 in mouse renal epithelia causes differentiation in vivo into cells expressing characteristic AML markers. Human renal AML and a renal AML cell line express proximal tubule markers. We describe the first mouse models of renal AML and provide evidence that these mesenchymal tumours originate from renal proximal tubule epithelial cells, uncovering an unexpected pathological differentiation plasticity of the proximal tubule.
肾血管平滑肌脂肪瘤(AML)含有多种不同间充质谱系克隆肿瘤细胞的混合物,提示存在未识别的 AML 肿瘤干细胞。TSC2 或 TSC1 的双等位基因失活被认为是这些肿瘤的驱动事件。在这里,我们表明 TSC2 敲低将衰老抗性培养的小鼠和人肾上皮细胞转化为成瘤性干细胞,这些干细胞在小鼠中连续增殖肾 AML 样肿瘤。mTOR 抑制治疗小鼠 AML 同种异体移植物模拟了人类肾 AML 的临床反应。在小鼠肾上皮细胞中删除 Tsc1 会导致体内分化为表达特征性 AML 标志物的细胞。人肾 AML 和肾 AML 细胞系表达近端小管标记物。我们描述了肾 AML 的首个小鼠模型,并提供证据表明这些间叶性肿瘤源自肾近端小管上皮细胞,揭示了近端小管的意外病理分化可塑性。