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A549 cells are adenocarcinomic human alveolar basal epithelial cells, and constitute a cell line that was first developed in 1972 by D. J. Giard, et al. through the removal and culturing of cancerous lung tissue in the explanted tumor of a 58-year-old caucasian male. [1]
Most immortalised cell lines are classified by the cell type they originated from or are most similar to biologically 3T3 cells – a mouse fibroblast cell line derived from a spontaneous mutation in cultured mouse embryo tissue. A549 cells – derived from a cancer patient lung tumor
To further confirm that endogenous wild-type p53 is really causing the repression of survivin gene expression, the authors induced A549 (human lung cancer cell line with wild-type p53) and T47D (human breast cancer cell line with mutant p53) cells with DNA-damaging agent adriamycin to trigger the physiological p53 apoptotic response in these ...
Lewis lung carcinoma is a hypermutated Kras/Nras–mutant cancer with extensive regional mutation clusters in its genome. A tumor that spontaneously developed as an epidermoid carcinoma in the lung of a C57BL mouse. It was discovered in 1951 by Dr. Margaret Lewis of the Wistar Institute and became one of the first transplantable tumors. [1]
C) A549 cells treated with a short hairpin RNA that knocked down their levels of SUCNR1 had significantly reduced migration responses to succinate. D) A549 cells treated with succinate showed increases in SNAI1, a transcription factor that promotes EMT. E) Metformin (which is an inhibitor of EMT [72]) abolished the migration responses of A549 ...
Meanwhile, the overexpression of miR-26a in the A549 human lung cancer cell line dramatically inhibits cell proliferation, blocks G1/S phase transition, induces apoptosis, and inhibits cell metastasis and invasion in vitro. Enhancer of zeste homolog 2 (EZH2) is a potential target of miR-26a. [19] Glioma
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