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A549 Cell - Crossref

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Last Updated: 10 June 2022

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RETRACTED ARTICLE: Effect of Paclitaxel-Mesoporous Silica Nanoparticles with a Core-Shell Structure on the Human Lung Cancer Cell Line A549

The value of PAC-csMSN used for respiratory delivery in rabbits was 2. 678-fold higher than that obtained with the PAC. " Cell apoptosis results obtained by flow cytometry showed that PAC-csMSN was more potent than pure PAC in promoting cell apoptosis. Transmission electron microscopy and laser scanning confocal microscopy carried out an absorption study of PAC-csMSN in A549 cells. These results show that csMSN has the ability to provide pulmonary inhalation therapy of lung cancer by poorly water-soluble drugs.

Source link: https://doi.org/10.1186/s11671-017-1826-1


Abstract A156: CrkI and CrkII adaptor proteins promote invasiveness and metastasis via epithelial-mesenchymal transition (EMT) in A549 lung adenocarcinoma cells.

"Similarly, Crk adaptor proteins were shown to promote an epithelial-mesenchymal-like transition and are essential for HGF-mediated cell proliferation and epithelial junction breakdown in MDCK kidney epithelial cells. " In vitro and in vivo, we show that overexpression of CrkI and CrkII occurs in this study; members of Crk adaptor families of signalling proteins in A549 lung adenocarcinoma cells promote morphological changes that mimic mesenchymal cells with high motility and invasiveness potential in both in vitro and in vivo.

Source link: https://doi.org/10.1158/1535-7163.targ-13-a156


A highly epothilone B–resistant A549 cell line with mutations in tubulin that confer drug dependence

"Abstract A 95-fold epothilone B u2013-resistant, but not dependent A549 human lung carcinoma cell line A549A/B40 have a Gln to Glu mutation at residue 292 near the M-loop of u03b2I-tubulin. A549. EpoB480, which is u223C900-fold resistant to EpoB, is a further selection of this cell line with higher amounts of EpoB. The u03b2-tubulin and Ku03b11-tubulin genes in EpoB480 revealed that in comparison to the b2292 mutation, a u03b260 was mutated from Val to Phe, with Leu to Met, and a mutated from Leu to Met, as shown by Sequence analysis. U03b1195 is located at the external surface of the microtubule, which has been suggested as the domain that communicates with a variety of endogenous proteins, such as stathmin and microtubule-associated protein 4. A mutation at u03b1195 may alter tubulin and regulatory proteins' interactions.

Source link: https://doi.org/10.1158/1535-7163.mct-05-0024


Silibinin inhibits cytokine-induced signaling cascades and down-regulates inducible nitric oxide synthase in human lung carcinoma A549 cells

"Abstract" is a fictional word that refers to the development and progression of primary lung tumor formation in mice and down-regulates inducible nitric oxide synthase expression in tumors, according to a literature review; however, the mechanisms of silibinin action are unclear. Also, signaling pathways that promote several transcription factors that are associated with lung carcinogenesis and their inhibition may be a cost-effective way to prevent and/or treat lung cancer. We used human lung epithelial carcinoma A549 cells to investigate the potential mechanisms, and a high iNOS cytokine mixture was observed. In the presence or absence of a cytokine mixture, silibininin therapy reduced constitutive phosphorylation. These results indicate that silibinin may have multiple cytokine-induced signaling pathways to down-regulate iNOS expression in lung cancer cells, which could contribute to its overall cancer prevention success against lung tumorigenesis. ".

Source link: https://doi.org/10.1158/1535-7163.mct-08-0256


Water Soluble and Insoluble Components of PM2.5 in Nanchang City and Their Cytotoxic Research on Epithelial Cells (A549)

"Abstract": "Abstract" investigates PM 2. 5's adverse effects on human lung epithelial cells A549 and the potential mechanism of action, this research seeks to identify water-soluble and insoluble components of PM 2. 5 by gathering atmospheric fine particles. The MTT method, which measured the cell survival rate, converted the desiccated PM 2. 5 into water-soluble and insoluble components, assessed the cell toxicity of WS-PM 2. 5 and WIS-PM 2. 5. Cell reactive oxygen species were characterized by flow cytometry, and the expression of cell inflammatory genes IL-6 and TNF-u03b1 were determined by ELISA and RT-QPCR. WIS-PM 2. 5 has shown to be significantly larger than that of WS-PM 2. 5 in inhibiting cell viability, cell membrane damage, and oxidative stress, while still significantly less than WS-PM 2. 5 in causing inflammatory damage," the tester says.

Source link: https://doi.org/10.21203/rs.3.rs-1660578/v1


Lysophosphatidic Acid Decreases the Nuclear Localization and Cellular Abundance of the p53 Tumor Suppressor in A549 Lung Carcinoma Cells

"Abstract Lysophosphatidic acid is a bioactive lipid that promotes cancer cell proliferation and motility by stimulating cell proliferation and motility by stimulating cell proliferation and motility by stimulation of cell surface G proteinu2013coupled receptors. " We first report that LPA reduces the cellular abundance of the tumor suppressor p53 in A549 lung carcinoma cells, which express endogenous LPA receptors. Cells of A549 cells were partially covered by actinomycin D induction of both apoptosis and increased p53 abundance in LPA cells. These results establish p53 as a point of LPA action and provide a new insight into how LPA promotes cancer cell division, shields against apoptosis, and thus promotes tumor formation. ".

Source link: https://doi.org/10.1158/1541-7786.mcr-06-0338


CCAAT Enhancer Binding Protein-β Regulates Matrix Metalloproteinase-1 Expression in Interleukin-1β–Stimulated A549 Lung Carcinoma Cells

"Abstract Matrix Metalloproteinase-1 is an inflammation-inducible neutral protease that mediates extracellular matrix remodeling and promotes tumor invasion. " We investigated the activation of MMP-1 gene expression in A549 lung carcinoma cells stimulated with the inflammatory cytokine interleukin-1 (u03b2) in this study. MMP-1 mRNA levels were highest after 16 hours of IL-1u03b2 stimulation, which was correlated with the expression of the transcription factor CCAAT enhancer-binding protein-u03b2. We found that MMP-1 mRNA levels were maximal following 16 hours of IL-1u03b2 stimulation, which was correlated with the expression of the transcription factor CCAAT enhancer-binding protein-u03b2-u03b2 u03b2 mRNA levels were u03b2 production. CEBPB binds to this promoter element maximally 16 hours after IL-1u03b2 stimulation, according to electrophoresis mobility shift assays. The LAP1, LAP2, and LIP isoforms of CEBPB bind to the IL-1304, MMP-1 promoter, according to DNA affinity chromatography results, which confirmed that the LAP1, LAP2, and LIP isoforms of CEBPB bind to the CEBPB's MMP-1 promoter's MMP-1 promoter. These findings establish CEBPB as a key mediator of inflammatory responses in lung cancer cells and highlight the numerous regulatory roles of CEBPB isoforms.

Source link: https://doi.org/10.1158/1541-7786.mcr-09-0082


Gallic Acid Suppresses Lipopolysaccharide-Induced Nuclear Factor-κB Signaling by Preventing RelA Acetylation in A549 Lung Cancer Cells

"Abstract" is a word that refers to a host of malignant change, cancer formation, and inflammation, according to several studies, gallic acid plays a vital role in the reduction of malignant transformation, tumor formation, and inflammation. " However, the exact mechanism of gallic acid in inflammatory diseases is also unclear. Gallic acid from Rosa rugosa was identified as a global regulator with global specificity for the majority of HAT enzymes, but not active against epigenetic enzymes such as sirtuin 1, histone deacetylase, and histone methyltransferase. In vivo, we've also demonstrated that gallic acid treatment reduces the acetylation of p65 and the LPS-induced serum levels of interleukin-6.

Source link: https://doi.org/10.1158/1541-7786.mcr-09-0239


Hypoxia Enhances Sphingosine Kinase 2 Activity and Provokes Sphingosine-1-Phosphate-Mediated Chemoresistance in A549 Lung Cancer Cells

"While HIF-1 is commonly agreed that it aids tumor cell proliferation and tissue expression under hypoxia, HIF-1-independent mechanisms function as well. " We have evidence that conditioned medium obtained from A549 cells, which were incubated for 24 hours under hypoxia, shielded naive A549 cells from etoposide-induced cell death in vivas. More specifically, the bioactive lipid sphingosine-1-phosphate not only was critical for cell viability of A549 cells but also shielded cells from apoptosis. Under hypoxia, we observed an increase in sphingosine kinase 2 protein level and enzyme production, which was likely due to the introduction of S1P into the medium. "Specific small interfering RNA reduced A549 cells under hypoxia and conditioned medium obtained from SphK2 knockdown cells was only partially protective," said the chemoresistance of A549 cells under hypoxia and conditioned medium obtained from SphK2 knockdown cells was only partially protective. ".

Source link: https://doi.org/10.1158/1541-7786.mcr-08-0156


Effect of TEI-6720, a Xanthine Oxidase Inhibitor, on the Nucleoside Transport in the Lung Cancer Cell Line A549

"TEI-6720 inhibited the production of xanthine oxidase in A549 cells, but did not affect other enzymes," the manufacturer reported. TEI-6720 was not only preventing a decrease in the inosine content in inosine-containing medium but also a decrease in the uridine concentration in uridine-containing medium during incubation. These results show that TEI-6720 is a catalyst for the Na-independent nucleoside transport of uridine and inosine, as well as xanthine oxidase. ".

Source link: https://doi.org/10.1159/000028344

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions