JCI：邪恶的肿瘤细胞“劫持”周围组织，导致其快速生长

肿瘤的生长依赖于其癌症细胞和周围正常组织或者癌症基座的相互作用，间质细胞可以刺激肿瘤细胞的生长，然而，目前是否肿瘤细胞可以影响其基座细胞并不清楚。

刊登在9月一期的国际杂志<em>Journal of Clinical Investigation</em>上的一年研究报告中，来自安德森癌症研究中心的研究者报道了，卵巢癌细胞可以激活HOXA9基因来强迫基座细胞产生可供肿瘤生长发育的环境。

<!--more-->

研究者Honami Naora和其同事发现，在卵巢癌病人和小鼠模型中，HOXA9基因的表达和病人治疗结果失败直接关联，卵巢癌细胞中HOXA9基因的表达可以促使细胞产生一种名为TGF-β的蛋白质，该蛋白质随后会诱导周围的非癌性细胞产生供肿瘤发育的环境。通过在卵巢癌细胞中阻碍TGF-β的表达可以明显降低肿瘤细胞的生长。

这项研究发现为我们提供了思路，我们可以以TGF-β为靶点来开发出治疗卵巢癌的新型药物。

编译自：<a title="" href="http://www.sciencedaily.com/releases/2012/09/120904121436.htm" target="_blank">Ovarian Cancer Cells Hijack Surrounding Tissues to Enhance Tumor Growth</a>
<div id="ztload">
<div>
<div>

<img src="http://www.bioon.com/biology/UploadFiles/201209/2012090522321457.jpg" alt="" width="113" height="149" border="0" />

<a title="" href="http://dx.doi.org/doi:10.1172/JCI62229" target="_blank">doi:10.1172/JCI62229</a>
PMC:
PMID:

</div>
<div>

<br/><strong>HOXA9 promotes ovarian cancer growth by stimulating cancer-associated fibroblasts</strong><br/>


Ko SY, Barengo N, Ladanyi A, Lee JS, Marini F, Lengyel E, Naora H.

Epithelial ovarian cancers (EOCs) often exhibit morphologic features of embryonic Müllerian duct-derived tissue lineages and colonize peritoneal surfaces that overlie connective and adipose tissues. However, the mechanisms that enable EOC cells to readily adapt to the peritoneal environment are poorly understood. In this study, we show that expression of HOXA9, a Müllerian-patterning gene, is strongly associated with poor outcomes in patients with EOC and in mouse xenograft models of EOC. Whereas HOXA9 promoted EOC growth in vivo, HOXA9 did not stimulate autonomous tumor cell growth in vitro. On the other hand, expression of HOXA9 in EOC cells induced normal peritoneal fibroblasts to express markers of cancer-associated fibroblasts (CAFs) and to stimulate growth of EOC and endothelial cells. Similarly, expression of HOXA9 in EOC cells induced normal adipose- and bone marrow-derived mesenchymal stem cells (MSCs) to acquire features of CAFs. These effects of HOXA9 were due in substantial part to its transcriptional activation of the gene encoding TGF-β2 that acted in a paracrine manner on peritoneal fibroblasts and MSCs to induce CXCL12, IL-6, and VEGF-A expression. These results indicate that HOXA9 expression in EOC cells promotes a microenvironment that is permissive for tumor growth.

<br/>来源：生物谷

</div>
</div>
</div>