Tumor Microenvironment and Metastasis Program.
Mol Cell Proteomics. 2013 Dec;12(12):3778-92. doi: 10.1074/mcp.M113.029587. Epub 2013 Sep 13.
Epithelial-mesenchymal transition (EMT) is a key contributor in tumor progression and metastasis. EMT produces cellular heterogeneity within head and neck squamous cell carcinomas (HNSCC) by creating a phenotypically distinct mesenchymal subpopulation that is resistant to conventional therapies. In this study, we systematically characterized differences in the secretomes of E-cadherin high epithelial-like and E-cadherin low mesenchymal-like subpopulations using unbiased and targeted proteomics. A total 1765 proteins showed significant changes with 177 elevated in the epithelial subpopulation and 173 elevated in the mesenchymal cells. Key nodes in affected networks included NFκB, Akt, and ERK, and most implicated cellular components involved various aspects of the extracellular matrix. In particular, large changes were observed in multiple collagens with most affected collagens at much higher abundance levels in the mesenchymal subpopulation. These cells also exhibited a secretome profile resembling that of cancer-associated fibroblastic cells (CAF). S100A4, a commonly used marker for cancer-associated fibroblastic cells, was elevated more than 20-fold in the mesenchymal cells and this increase was further verified at the transcriptome level. S100A4 is a known mediator of EMT, leading to metastasis and EMT has been proposed as a potential source of cancer-associated fibroblastic cells in solid tumors. S100A4 knockdown by small interfering RNA led to decreased expression, secretion and activity of matrix metalloproteinase 2, as verified by quantitative PCR, multiple reaction monitoring and zymography analyses, and reduced invasion in collagen-embedded spheroids. Further confirmation in three-dimensional organotypic reconstructs showed less invasion and advanced differentiation in the S100A4 RNA interference samples. Orthotopic metastasis model, developed to validate the findings in vivo, demonstrated a decrease in spontaneous metastasis and augmented differentiation in the primary tumor in siS100A4 xenografts. These results demonstrate the value of secretome profiling to evaluate phenotypic conversion and identify potential novel therapeutic targets such as S100A4.
上皮-间充质转化 (EMT) 是肿瘤进展和转移的关键因素。EMT 通过产生表型上明显不同的间充质亚群,使头颈部鳞状细胞癌 (HNSCC) 内的细胞异质性产生,而这些细胞对传统疗法具有抗性。在这项研究中,我们使用无偏和靶向蛋白质组学系统地描述了 E-钙黏蛋白高上皮样和 E-钙黏蛋白低间充质样亚群的分泌组之间的差异。有 1765 种蛋白质显示出显著变化,其中 177 种在上皮亚群中升高,173 种在间充质细胞中升高。受影响网络中的关键节点包括 NFκB、Akt 和 ERK,最受牵连的细胞成分涉及细胞外基质的各个方面。特别是,多种胶原蛋白发生了巨大变化,其中大多数受影响的胶原蛋白在间充质亚群中的丰度水平更高。这些细胞还表现出与癌症相关成纤维细胞 (CAF) 相似的分泌组谱。S100A4 是癌症相关成纤维细胞的常用标志物,在间充质细胞中升高了 20 多倍,这一增加在转录组水平上进一步得到了验证。S100A4 是 EMT 的已知介质,导致转移和 EMT 已被提议为实体瘤中癌症相关成纤维细胞的潜在来源。通过小干扰 RNA 敲低 S100A4 导致基质金属蛋白酶 2 的表达、分泌和活性降低,这通过定量 PCR、多重反应监测和胶凝电泳分析得到了验证,并减少了胶原包埋球体中的侵袭。在三维器官型重建中的进一步验证表明,S100A4 RNA 干扰样品的侵袭减少和分化程度更高。为了在体内验证这些发现而开发的原位转移模型表明,siS100A4 异种移植物中的自发转移减少和原发肿瘤中的分化增强。这些结果证明了分泌组谱分析在评估表型转化和鉴定潜在的新治疗靶点(如 S100A4)方面的价值。