Abstract
BackgroundA tumor is considered a heterogeneous complex in a three-dimensional environment that is flush with pathophysiological and biomechanical signals. Cell-stroma interactions guide the development and generation of tumors. Here, we evaluate the contributions of normal fibroblasts to gastric cancer.Methodology/Principal FindingsBy coculturing normal fibroblasts in monolayers of BGC-823 gastric cancer cells, tumor cells sporadically developed short, spindle-like morphological characteristics and demonstrated enhanced proliferation and invasive potential. Furthermore, the transformed tumor cells demonstrated decreased tumor formation and increased lymphomatic and intestinal metastatic potential. Non-transformed BGC-823 cells, in contrast, demonstrated primary tumor formation and delayed intestinal and lymph node invasion. We also observed E-cadherin loss and the upregulation of vimentin expression in the transformed tumor cells, which suggested that the increase in metastasis was induced by epithelial-to-mesenchymal transition.ConclusionCollectively, our data indicated that normal fibroblasts sufficiently induce epithelial-to-mesenchymal transition in cancer cells, thereby leading to metastasis.
Highlights
Metastases are responsible for up to 90% of cancer-associated mortality
Collectively, our data indicated that normal fibroblasts sufficiently induce epithelial-to-mesenchymal transition in cancer cells, thereby leading to metastasis
For the generation of the transformed BGC-823 cells (TBGCs), the fibroblasts (FBs) and BGC-823 cells were cocultured at a ratio of 10:1 for an additional 10 days after the cultured cells reached confluence
Summary
Metastases are responsible for up to 90% of cancer-associated mortality. Many patients who demonstrate no evidence of metastasis at the initial diagnosis will eventually develop metastasis. Metastases cause most cancer deaths, this process remains one of the most enigmatic aspects of the disease. Metastatic tumor cells enter tissue via extravasation. The tissue, undergoes unclear processes by which the cells are imbedded in the tissue matrix and come into direct contact with stromal cells, most of which are normal fibroblasts. Tumor cells have every chance to come into contact with stromal cells, including neoplastic and metastatic cells [1]. This leads to reciprocal cross-talk with normal fibroblasts in the tissue. Cell-stroma interactions guide the development and generation of tumors. We evaluate the contributions of normal fibroblasts to gastric cancer
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