![]() Beside the loss of epithelial markers the expression of mesenchymal markers like FSP-1 is also an important step in the process of EMT. The process of EMT is associated with a loss of E-cadherin, which is positively correlated with tumor stage and poor survival in many epithelial tumor –. One of the most important molecular markers of epithelial cells is the epithelial adhesion molecule E-cadherin, mediating cell-cell interactions. In addition to morphological changes, the process of EMT is characterized by differences in transcription and expression of epithelial and mesenchymal genes. EMT is a complex multistep event, which changes not only cell morphology but also enables cells to gain important new functions like the expression of new molecules or migration and invasion. Although still under debate, epithelial to mesenchymal transition (EMT) seems to be one of the key events in local progress and metastasis of epithelial malignancies. Tumor metastasis is a complex event involving multiple steps including separation of cancer cells from the compact primary tumor, migration into vessels, invasion in tissue and formation of a secondary tumor nodule. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials. There are no further patents, products in development or marketed products to declare. have applied for a patent on CCL18 and CCL18R as biomarker and therapy target (patent pending). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have the following interests. is a recipient of a grant by the Albert-Ludwig University Freiburg (Stiftung Mattern). This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: There are no current external funding sources for this study. Received: JAccepted: NovemPublished: January 18, 2013Ĭopyright: © 2013 Ploenes et al. PLoS ONE 8(1):Ĭincinnati Children's Hospital Medical Center, United States of America (2013) CC-Chemokine Ligand 18 Induces Epithelial to Mesenchymal Transition in Lung Cancer A549 Cells and Elevates the Invasive Potential. Therefore, CCL18 may be an interesting therapeutic target for NSCLC.Ĭitation: Ploenes T, Scholtes B, Krohn A, Burger M, Passlick B, Müller-Quernheim J, et al. In addition, CCL18 induced chemotaxis of these cells and increased their chemoresistance. In contrast, an increasing CCL18 concentration was associated with a decline of cell proliferation rate. Accordingly, CCL18 induced the transcriptional EMT regulator SNAIL1 in a dose dependent fashion. Exposure of A549 lung cancer cells to CCL18 in various concentrations decreases the epithelial marker E-cadherin, whereas FSP-1, a marker of the mesenchymal phenotype increases. We investigated the effect of CCL18 on A549, an adenocarcinoma cell line of the lung, on EMT and other cell functions like proliferation, chemotaxis, invasion, chemoresistance and proliferation. Therefore, we hypothesized that CCL18 may be directly involved in pathological processes of lung cancer, e.g. We already demonstrated that serum levels of CCL18, a primate specific chemokine, are highly elevated in patients with lung cancer and correlate with their survival time of patients with adenocarcinoma of the lung. Although the exact mechanisms are still unknown, the process of epithelial to mesenchymal transition (EMT) seems to be involved in these neoplastic processes. The poor prognosis is due to its high aggressiveness and its early metastasis. Lung cancer is one of the leading causes of cancer related death worldwide with more than a million deaths per year.
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