Colmone Angela, Amorim Maria, Pontier Andrea L, Wang Sheng, Jablonski Elizabeth, Sipkins Dorothy A
Department of Medicine, Section of Hematology/Oncology, University of Chicago, 5841 South Maryland Avenue MC 2115, Chicago, IL 60637, USA.
Science. 2008 Dec 19;322(5909):1861-5. doi: 10.1126/science.1164390.
The host tissue microenvironment influences malignant cell proliferation and metastasis, but little is known about how tumor-induced changes in the microenvironment affect benign cellular ecosystems. Applying dynamic in vivo imaging to a mouse model, we show that leukemic cell growth disrupts normal hematopoietic progenitor cell (HPC) bone marrow niches and creates abnormal microenvironments that sequester transplanted human CD34+ (HPC-enriched) cells. CD34+ cells in leukemic mice declined in number over time and failed to mobilize into the peripheral circulation in response to cytokine stimulation. Neutralization of stem cell factor (SCF) secreted by leukemic cells inhibited CD34+ cell migration into malignant niches, normalized CD34+ cell numbers, and restored CD34+ cell mobilization in leukemic mice. These data suggest that the tumor microenvironment causes HPC dysfunction by usurping normal HPC niches and that therapeutic inhibition of HPC interaction with tumor niches may help maintain normal progenitor cell function in the setting of malignancy.
宿主组织微环境影响恶性细胞的增殖和转移,但对于肿瘤诱导的微环境变化如何影响良性细胞生态系统却知之甚少。通过对小鼠模型应用动态体内成像技术,我们发现白血病细胞的生长破坏了正常造血祖细胞(HPC)的骨髓龛,并创造了异常微环境,隔离了移植的人类CD34+(富含HPC)细胞。白血病小鼠体内的CD34+细胞数量随时间下降,并且在细胞因子刺激下未能动员到外周循环中。中和白血病细胞分泌的干细胞因子(SCF)可抑制CD34+细胞迁移到恶性龛中,使CD34+细胞数量正常化,并恢复白血病小鼠中CD34+细胞的动员。这些数据表明,肿瘤微环境通过篡夺正常HPC龛导致HPC功能障碍,并且对HPC与肿瘤龛相互作用的治疗性抑制可能有助于在恶性肿瘤情况下维持正常祖细胞功能。