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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]
miR-26a plays an important role as an anti-oncogene in the molecular mechanism of human lung cancer. miR-26a expression is down-regulated in human lung cancer tissues relative to normal tissues. Meanwhile, the overexpression of miR-26a in the A549 human lung cancer cell line dramatically inhibits cell proliferation, blocks G1/S phase transition ...
2) GW9508 reduced the motility of A549 human lung cancer cells; GW9508 plus GW1100 treatment of these cells further reduced their motility; FFAR1 gene knockdown A549 cells showed less motility than control A549 cells; and GW9508-treated A549 FFAR1 gene knockdown cells had less motility than control or GW9508-treated cells.
The panel holds cell lines representing leukemia, melanoma, non-small-cell lung carcinoma, and cancers of the brain, ovary, breast, colon, kidney, and prostate. [1] [2]13 additional cell lines are evaluated for use in the screening program, among them two lines deriving from so far not represented small-cell lung carcinoma.
[69] 4) Butyric acid inhibited the proliferation of and triggered apoptosis in cultured human A549 lung cancer cells; [70] further studies in A549 as well as H1299 human lung cancer cells found that propionic acid inhibited their stimulated migration, invasiveness, and colony growth in cell culture assays but did not do so in FFAR2 gene ...
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 ...
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