13 research outputs found
Manipulating the Optical Properties of Carbon Dots by Fine-Tuning their Structural Features
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Long non-coding RNA CHCHD4P4 promotes epithelial-mesenchymal transition and inhibits cell proliferation in calcium oxalate-induced kidney damage
Acute fibrinous and organizing pneumonia associated with influenza A/H1N1 pneumonia after lung transplantation
CC Chemokin ligand 18 (CCL18) induziert Chemotaxis und phenotypische Veränderungen bei der Lungenkarzinomzelllinie A549
Serumkonzentrationen des CC Chemokin ligand 18 (CCL18) beim nichtkleinzelligen Lungenkarzinom
Die Serumkonzentration des CC Chemokin ligand 18 (CCL18) ist bei Patienten mit Nicht-kleinzelligem Lungenkarzinom erhöht und korreliert mit der Überlebenszeit
CCL18 promotes the invasion and migration of gastric cancer cells via ERK1/2/NF-κB signaling pathway
Chronic intermittent abdominal pain in young woman with intestinal malrotation, Fitz-Hugh-Curtis Syndrome and appendiceal neuroendocrine tumor: a rare case report and literature review
Efficacy of phase 1 trials in malignant pleural mesothelioma: Description of a series of patients at a single institution
Tumor Cell Heterogeneity in Small Cell Lung Cancer (SCLC): Phenotypical and Functional Differences Associated with Epithelial-Mesenchymal Transition (EMT) and DNA Methylation Changes
Small Cell Lung Cancer (SCLC) is a specific subtype of lung cancer presenting as highly metastatic disease with extremely poor prognosis. Despite responding initially well to chemo- or radiotherapy, SCLC almost invariably relapses and develops resistance to chemotherapy. This is suspected to be related to tumor cell subpopulations with different characteristics resembling stem cells. Epithelial-Mesenchymal Transition (EMT) is known to play a key role in metastatic processes and in developing drug resistance. This is also true for NSCLC, but there is very little information on EMT processes in SCLC so far. SCLC, in contrast to NSCLC cell lines, grow mainly in floating cell clusters and a minor part as adherent cells. We compared these morphologically different subpopulations of SCLC cell lines for EMT and epigenetic features, detecting significant differences in the adherent subpopulations with high levels of mesenchymal markers such as Vimentin and Fibronectin and very low levels of epithelial markers like E-cadherin and Zona Occludens 1. In addition, expression of EMT-related transcription factors such as Snail/Snai1, Slug/Snai2, and Zeb1, DNA methylation patterns of the EMT hallmark genes, functional responses like migration, invasion, matrix metalloproteases secretion, and resistance to chemotherapeutic drug treatment all differed significantly between the sublines. This phenotypic variability might reflect tumor cell heterogeneity and EMT during metastasis in vivo, accompanied by the development of refractory disease in relapse. We propose that epigenetic regulation plays a key role during phenotypical and functional changes in tumor cells and might therefore provide new treatment options for SCLC patients