Spenlé Caroline, Gasser Isabelle, Saupe Falk, Janssen Klaus-Peter, Arnold Christiane, Klein Annick, van der Heyden Michael, Mutterer Jérome, Neuville-Méchine Agnès, Chenard Marie-Pierre, Guenot Dominique, Esposito Iréne, Slotta-Huspenina Julia, Ambartsumian Noona, Simon-Assmann Patricia, Orend Gertraud
a Inserm U1109 ; The Microenvironmental Niche in Tumorigenesis and Targeted Therapy ; (MN3T) ; Strasbourg , France.
Cell Adh Migr. 2015;9(1-2):4-13. doi: 10.1080/19336918.2015.1005452.
The extracellular matrix (ECM) molecule tenascin-C (TNC) promotes tumor progression. This has recently been demonstrated in the stochastic murine RIP1-Tag2 insulinoma model, engineered to either express TNC abundantly or to be devoid of TNC. However, our knowledge about organization of the TNC microenvironment is scant. Here we determined the spatial distribution of TNC together with other ECM molecules in murine RIP1-Tag2 insulinoma and human cancer tissue (insulinoma and colorectal carcinoma). We found that TNC is organized in matrix tracks together with other ECM molecules of the AngioMatrix signature, a previously described gene expression profile that characterizes the angiogenic switch. Moreover, stromal cells including endothelial cells, fibroblasts and leukocytes were enriched in the TNC tracks. Thus, TNC tracks may provide niches for stromal cells and regulate their behavior. Given similarities of TNC rich niches for stromal cells in human insulinoma and colon cancer, we propose that the RIP1-Tag2 model may be useful for providing insights into the contribution of the tumor stroma specific ECM as promoter of cancer progression.
细胞外基质(ECM)分子腱生蛋白-C(TNC)可促进肿瘤进展。最近在随机构建的小鼠RIP1-Tag2胰岛素瘤模型中得到了证实,该模型被设计为要么大量表达TNC,要么不含TNC。然而,我们对TNC微环境的组织情况了解甚少。在此,我们确定了TNC与其他ECM分子在小鼠RIP1-Tag2胰岛素瘤和人类癌症组织(胰岛素瘤和结肠直肠癌)中的空间分布。我们发现,TNC与血管生成基质特征的其他ECM分子一起形成基质轨道,血管生成基质特征是一种先前描述的表征血管生成转换的基因表达谱。此外,包括内皮细胞、成纤维细胞和白细胞在内的基质细胞在TNC轨道中富集。因此,TNC轨道可能为基质细胞提供生态位并调节其行为。鉴于人类胰岛素瘤和结肠癌中富含TNC的基质细胞生态位具有相似性,我们认为RIP1-Tag2模型可能有助于深入了解肿瘤基质特异性ECM作为癌症进展促进因子的作用。