Department of Chemical and Biological Engineering, The BioFrontiers Institute, University of Colorado at Boulder, 3415 Colorado Ave, 596 UCB, Boulder, CO, 80303, USA.
Department of Molecular, Cellular, and Developmental Biology, BioFrontiers Institute, University of Colorado, Boulder, CO, 80309, USA.
Biomaterials. 2018 Feb;155:124-134. doi: 10.1016/j.biomaterials.2017.11.008. Epub 2017 Nov 15.
Interactions between lung epithelium and interstitial fibroblasts are increasingly recognized as playing a major role in the progression of several lung pathologies, including cancer. Three-dimensional in vitro co-culture systems offer tissue-relevant platforms to study the signaling interplay between diseased and healthy cell types. Such systems provide a controlled environment in which to probe the mechanisms involved in epithelial-mesenchymal crosstalk. To recapitulate the native alveolar tissue architecture, we employed a cyst templating technique to culture alveolar epithelial cells on photodegradable microspheres and subsequently encapsulated the cell-laden spheres within poly (ethylene glycol) (PEG) hydrogels containing dispersed pulmonary fibroblasts. A fibroblast cell line (CCL-210) was co-cultured with either healthy mouse alveolar epithelial primary cells or a cancerous alveolar epithelial cell line (A549) to probe the influence of tumor-stromal interactions on proliferation, migration, and matrix remodeling. In 3D co-culture, cancerous epithelial cells and fibroblasts had higher proliferation rates. When examining fibroblast motility, the fibroblasts migrated faster when co-cultured with cancerous A549 cells. Finally, a fluorescent peptide reporter for matrix metalloproteinase (MMP) activity revealed increased MMP activity when A549s and fibroblasts were co-cultured. When MMP activity was inhibited or when cells were cultured in gels with a non-degradable crosslinker, fibroblast migration was dramatically suppressed, and the increase in cancer cell proliferation in co-culture was abrogated. Together, this evidence supports the idea that there is an exchange between the alveolar epithelium and surrounding fibroblasts during cancer progression that depends on MMP activity and points to potential signaling routes that merit further investigation to determine targets for cancer treatment.
肺上皮细胞与间质成纤维细胞之间的相互作用越来越被认为在几种肺部疾病的进展中起着重要作用,包括癌症。三维体外共培养系统为研究疾病和健康细胞类型之间的信号相互作用提供了相关组织的平台。这种系统提供了一个受控的环境,可以探究上皮-间充质相互作用中涉及的机制。为了再现天然肺泡组织的结构,我们采用了囊泡模板技术,将肺泡上皮细胞培养在可光降解的微球上,然后将载有细胞的球体包封在含有分散的肺成纤维细胞的聚乙二醇 (PEG) 水凝胶中。将成纤维细胞系 (CCL-210) 与健康的小鼠肺泡上皮原代细胞或癌变的肺泡上皮细胞系 (A549) 共培养,以探究肿瘤-基质相互作用对增殖、迁移和基质重塑的影响。在 3D 共培养中,癌变的上皮细胞和成纤维细胞具有更高的增殖率。当检查成纤维细胞的迁移能力时,当与癌变的 A549 细胞共培养时,成纤维细胞迁移得更快。最后,基质金属蛋白酶 (MMP) 活性的荧光肽报告显示,当 A549 细胞和成纤维细胞共培养时,MMP 活性增加。当 MMP 活性被抑制或细胞在含有不可降解交联剂的凝胶中培养时,成纤维细胞的迁移被显著抑制,共培养中癌细胞增殖的增加被消除。总之,这些证据支持这样一种观点,即在癌症进展过程中,肺泡上皮细胞与周围成纤维细胞之间存在一种相互作用,这种作用依赖于 MMP 活性,并指出了值得进一步研究的潜在信号途径,以确定癌症治疗的靶点。