Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA; Development, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Development, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Cell Rep. 2019 Jan 15;26(3):689-701.e6. doi: 10.1016/j.celrep.2018.12.089.
Most human cancers originate from high-turnover tissues, while low-proliferating tissues, like skeletal muscle, exhibit a lower incidence of tumor development. In Duchenne muscular dystrophy (DMD), which induces increased skeletal muscle regeneration, tumor incidence is increased. Rhabdomyosarcomas (RMSs), a rare and aggressive type of soft tissue sarcoma, can develop in this context, but the impact of DMD severity on RMS development and its cell of origin are poorly understood. Here, we show that RMS latency is affected by DMD severity and that muscle stem cells (MuSCs) can give rise to RMS in dystrophic mice. We report that even before tumor formation, MuSCs exhibit increased self-renewal and an expression signature associated with RMSs. These cells can form tumorspheres in vitro and give rise to RMSs in vivo. Finally, we show that the inflammatory genes Ccl11 and Rgs5 are involved in RMS growth. Together, our results show that DMD severity drives MuSC-mediated RMS development.
大多数人类癌症起源于高周转率组织,而增殖率低的组织,如骨骼肌,肿瘤发生的几率较低。在杜氏肌营养不良症(DMD)中,骨骼肌再生增加,肿瘤的发生率也会增加。横纹肌肉瘤(RMS)是一种罕见且侵袭性的软组织肉瘤,在这种情况下可以发展,但 DMD 严重程度对 RMS 发展及其起源细胞的影响尚不清楚。在这里,我们表明 RMS 的潜伏期受 DMD 严重程度的影响,并且肌肉干细胞(MuSCs)可以在营养不良的小鼠中产生 RMS。我们报告说,即使在肿瘤形成之前,MuSCs 就表现出了更高的自我更新能力和与 RMS 相关的表达特征。这些细胞可以在体外形成肿瘤球,并在体内产生 RMS。最后,我们表明炎症基因 Ccl11 和 Rgs5 参与了 RMS 的生长。总之,我们的研究结果表明,DMD 的严重程度会导致 MuSC 介导的 RMS 发展。