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A549 has also been employed in viral research and associated protein expression changes as a consequence of viral infection. [10] Although A549 is a cancer cell line, it has also been studied for its response to tuberculosis, specifically the production of chemokines as it is induced by the invading bacteria. [11]
An immortalised cell line is a population of ... A549 cells – derived from a cancer patient lung ... a widely used human cell line isolated from cervical cancer ...
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
Accordingly, the protein profile changes of human lung cancer cell lines A549 in response to periplocin treatment were investigated using proteomics approaches (2-DE combined with MS/MS) in conjunction with Western blot analysis to verify the changed proteins. [36]
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 ...
A549: Human: Lung: Human alveolar adenocarcinoma cell line - A549 cultured by MLM at different time points and cell numbers. [7] Immunohistochemistry (IHC) reveals epithelial markers on A549 after culturing in 3D with the MLM. Type II alveolar [7] Primary: Human: Lung: Human tracheal smooth muscle cells (HTSMCs) [7] Primary: Human: Lung
In cell culture studies, human A549 lung adenocarcinoma cells and Huh7 human hepatocyte-derived cancer cells were treated with buffer or 4-octyl itaconate for 2 days and then infected with Zika virus for 4 days. 4-Octyl itaconate suppressed the growth of this virus in both cancer cell types. [80]
In lung adenocarcinoma cell line A549 overexpression of IRS-1 leads to reduced growth. Tumor infiltrating neutrophils have recently been thought to adjust tumor growth and invasiveness. Neutrophil elastase is shown to degrade IRS-1 by gaining access to endosomal compartment of carcinoma cell. IRS-1 degradation induces cell proliferation in ...
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