腫瘤相關(guān)基質(zhì)細(xì)胞中的間質(zhì)細(xì)胞對腫瘤細(xì)胞的生物學(xué)行為發(fā)揮至關(guān)重要作用,。近日，Cancer Discovery雜志上刊登的一項最新研究重點研究了癌細(xì)胞與間質(zhì)干細(xì)胞（MSCs）之間的相互作用,，研究發(fā)現(xiàn)間質(zhì)干細(xì)胞被招募到腫瘤基質(zhì)中,，一旦到達(dá)腫瘤基質(zhì)就能夠影響腫瘤細(xì)胞的表型。
腫瘤細(xì)胞來源的白細(xì)胞介素1（IL-1）誘導(dǎo)間充質(zhì)干細(xì)胞分泌前列腺素E2（PGE2）,。PGE2自分泌的方式運作配合旁分泌的IL-1信號誘發(fā)間充質(zhì)干細(xì)胞大量細(xì)胞因子的表達(dá),。
PGE2及細(xì)胞因子然后以旁分泌的方式作用于腫瘤細(xì)胞，誘導(dǎo)β-catenin信號的激活以及癌癥干細(xì)胞的形成,。這些現(xiàn)象表明骨髓間充質(zhì)干細(xì)胞及其衍生細(xì)胞類型通過PGE2及細(xì)胞因子的釋放創(chuàng)建出一個癌癥干細(xì)胞微環(huán)境促使腫瘤向前發(fā)展,。（生物谷：Bioon.com）
doi:10.1158/2159-8290.CD-12-0101
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Cancer-stimulated mesenchymal stem cells create a carcinoma stem-cell niche via Prostaglandin E2 signaling
Hua-Jung Li1, Ferenc Reinhardt2, Harvey R. Herschman3 and Robert A Weinberg2
Mesenchymal cells of the tumor-associated stroma are critical determinants of carcinoma cell behavior. We focus here on interactions of carcinoma cells with mesenchymal stem cells (MSCs), which are recruited to the tumor stroma and, once present, are able to influence the phenotype of the carcinoma cells. We find that carcinoma cell-derived interleukin-1 (IL-1) induces prostaglandin E2 (PGE2) secretion by MSCs. The resulting PGE2 operates in an autocrine manner, cooperating with ongoing paracrine IL-1 signaling, to induce expression of a group of cytokines by the MSCs. The PGE2 and cytokines then proceed to act in a paracrine fashion on the carcinoma cells to induce activation of β-catenin signaling and formation of cancer stem cells. These observations indicate that MSCs and derived cell types create a cancer stem-cell niche to enable tumor progression via release of PGE2 and cytokines.
