Division of Gene Regulation, Institute for Advanced Medical Research, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
Carcinogenesis. 2011 Nov;32(11):1597-606. doi: 10.1093/carcin/bgr183. Epub 2011 Aug 8.
Although the existence of tumor-initiating cells (T-ICs) in several types of human cancer has been documented, the contribution of somatic stem cells to the development of T-ICs has remained unclear. Here, we show that normal mouse ovary contains epithelial cell adhesion molecule (EpCAM)-expressing stem-like cells that possess the ability to differentiate into cytokeratin 8 (CK8)-expressing epithelial progeny cells. Furthermore, RNA interference-mediated transient depletion of the tumor suppressor p53 followed by retrovirus-mediated transfer of c-Myc and K-Ras oncogenes in EpCAM-expressing ovarian stem-like cells resulted in the generation of ovarian T-ICs. The established ovarian T-ICs gave rise to hierarchically organized lethal tumors in vivo and were able to undergo peritoneal metastasis. Finally, subsequent RNA interference-mediated knockdown of p53 in tumor cells triggered the expansion of EpCAM-expressing stem-like tumor cells and induced further tumor growth. These data reveal a role for p53 in the development and expansion of ovarian stem-like tumor cells and subsequent malignant progression.
尽管已经证实几种类型的人类癌症中存在肿瘤起始细胞(T-ICs),但体细胞干细胞对 T-ICs 发展的贡献仍不清楚。在这里,我们表明正常的小鼠卵巢中含有上皮细胞黏附分子(EpCAM)表达的干细胞样细胞,具有分化为角蛋白 8(CK8)表达的上皮祖细胞的能力。此外,RNA 干扰介导的短暂性肿瘤抑制因子 p53 耗竭,随后在 EpCAM 表达的卵巢干细胞样细胞中逆转录病毒转导 c-Myc 和 K-Ras 癌基因,导致卵巢 T-IC 的产生。所建立的卵巢 T-IC 在体内产生了具有层次结构的致死性肿瘤,并能够发生腹膜转移。最后,随后在肿瘤细胞中进行 RNA 干扰介导的 p53 敲低,引发 EpCAM 表达的干细胞样肿瘤细胞的扩增,并诱导进一步的肿瘤生长。这些数据揭示了 p53 在卵巢干细胞样肿瘤细胞的发育和扩增以及随后的恶性进展中的作用。