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- W2320243014 abstract "Folate, act as an one-carbon units donator or acceptor, participate in numerous biochemical reactions. Because mammals can9t synthesize folic acid de novo, obtain from diet or from microbial breakdown in the gut is essential. Pathological study revealed that tumor cell expressing high level of folate receptors (FR) comparing to normal tissue. Therefore, exploring the application of folate-related physiological properties as an anticancer strategy arose worldwide interesting. Previous studies in lung cancer revealed a positive correlation in folate receptors overexpression and efficacy of antifolate chemotherapy. Here we describe prolong Alimta treatment would prompt lung cancer cell9s malignancy. Cultivation of lung cancer CL1-0, CL1-5, and A549 in low dose Alimta (15-30 ng/mL) for 2-3 weeks would dramatically cause cell morphology change . Compare to control cell with round and flat epithelial like morphology, low dose Alimta treated cells showed mesenchymal to amoeboid phenotype. Further examination of epithelial to mesenchymal transition (EMT) markers showed the expression level of N-cadherin, matrix metalloproteinase 1 (MMP-1) and matrix metalloproteinase 2 (MMP-2) increased. Associated with morphology and EMT marker changed, cell migration and invasion ability of those Alimta treated cells were 3 folds higher than control cells. Besides, evaluated drug sensitivity by sulforhodamine B (SRB) method showed that those alimta treated cells were more resistant to gefitinib. These prominent events provoked our interesting to investigate the mechanism involving in the oncogenic effect induced by low dose Alimta treatment. While examing EMT-related transcription factors, both Slug and SOX-9 expression increased significantly. These evidences indicated that the folate metabolism defect induced metastasis could through the SOX-9 and Slug mechanism. Citation Format: Chun-Te Ho, Tsan-Zon Liu, Yu-Ting Chou, Shih-Hsin Hsiao, Jun-Jen Liu. Folate metabolism defect induce invasion and Gefinitib resistance in lung cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4970. doi:10.1158/1538-7445.AM2013-4970 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend." @default.
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- W2320243014 date "2013-04-15" @default.
- W2320243014 modified "2023-09-27" @default.
- W2320243014 title "Abstract 4970: Folate metabolism defect induce invasion and Gefinitib resistance in lung cancer." @default.
- W2320243014 doi "https://doi.org/10.1158/1538-7445.am2013-4970" @default.
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