Abstract

Abstract Introduction: Epithelial-mesenchymal transition (EMT) is a process in which cells undergo a developmental switch from an epithelial to a mesenchymal phenotype. During the EMT, epithelial cells seem to acquire malignant properties, with changes in cell morphology, invasion, and migration capacity. Vimentin is one of EMT markers for cancer cells, and vimentin expression of epithelial cells has been reported to be associated with the malignant phenotype of cancer cells in vitro. Fibroblasts, especially cancer-associated myofibroblasts which express α-smooth muscle actin, may affect the malignant phenotype of cancer cells. Then, we examined the effect of fibroblasts on the vimentin expression of gastric cancer cells. Materials & Methods: A gastric cancer cell line, OCUM-2MD3, and 3 gastric fibroblasts, CaF1, CaF32, and CaF33 those are derived from gastric tumor, were used in this study. Serum-free conditioned medium (SF-CM) from gastric fibroblasts was collected and stored at −20°C. As a control, DMEM was used instead of SF-CM. Following the addition of SF-CM into OCUM-2MD3 cells for 3 days, vimentin expression of OCUM-2MD3 was analyzed by reverse transcription-PCR. Correlation between vimentin expression of cancer cells and α-smooth muscle actin expression of fibroblasts was analayzed by Pearson's correlation coefficient test. Results: Vimentin expression of gastric cancer cells was 2.3 fold, 1.1 fold, and 1.3 fold increased by addition of SF-CM from CaF1, CaF32, and CaF33, respectively. α-Smooth muscle actin expression of each fibroblasts from CaF1, CaF32, and CaF33 was 7.7 fold, 1.3 fold, and 2.1 fold higher compared to the normal fibroblasts, respectively. Gastric cancer cells showed EMT by SF-CM. A significant correlation (p=0.017) was found between the α-smooth muscle actin expression level of fibloblast and the vimentin expression level of cancer cells. Conclusions: Tumor-stromal myofibroblast may stimulate malignant phenotype of gastric cancer cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1003.

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