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A549 Lung cancer Cells - Crossref

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Last Updated: 23 April 2022

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Synthesis of Novel Conjugated Linoleic Acid (CLA)-Coated Superparamagnetic Iron Oxide Nanoparticles (SPIONs) for the Delivery of Paclitaxel with Enhanced In Vitro Anti-Proliferative Activity on A549 Lung Cancer Cells

The use of Superparamagnetic Iron Oxide Nanoparticles as a nanomedicine for Non-Small Cell Lung Carcinoma can result in safe delivery of anticancer drugs with minimal side-effects. With the CLA-coated PTX-SPIONs against a lung adenocarcinoma cell line after 72 h, with a reported cell viability of 17. 1%, an increased anti-proliferative action was also observed against a lung adenocarcinoma cell line. Increased proliferation of A549 cells in comparison to pristine PTX, according to CLA-coated PTX-SPIONs, compared to pure PTX, demonstrating the possibility of using the nanomedicine as an effective site-specific delivery device for enhanced therapeutic activity in NSCLC therapy.

Source link: https://doi.org/10.3390/pharmaceutics14040829


Evaluation of silica nanoparticles cytotoxicity (20-40 nm) on cancerous epithelial cell (A549) and fibroblasts cells of human normal lung fibroblast (MRC5)

MTT assay and scanning electron microscopy images AFTER 72 hours. Cells and Methods: In vitro, cytotoxicity of silica nanoparticles in 0. 6 -3 mg/ml doses were investigated on human lung epithelial and human fetal lung fibroblast cells in 0. 6 -3 mg/ml concentrations. In both types of cells, the cell viability was reduced by increasing the percentage of SiO2 NPs from 0. 6 to 3 mg/ml. In 1. 6 mg/ml dose, the half-maximal inhibitory concentration of SiO2 NPs on A549 cancer cells, the likelihood of survival is as high as it is: %46 for A549 cancer and %70 for MRC5 normal cells. Conclusion: SiO2 NP's cytotoxicity depends on the amount of SiO2 NP and the type of cells. In addition, SiO2 NP's cytotoxicity against cancer cells is higher than that of normal lung cells.

Source link: https://doi.org/10.18502/tkj.v12i4.5872


The Effects of Costus speciosus Root Extract on Cultured Human Lung Cancer Cells, A549

Because more than 80% of society believes in traditional medicine as its cure, more than 80% of patients are finding novel solutions for anticancer drugs. Human lung cancer cells were analyzed by this study. The cell viability was reduced significantly by the treatment of cells with ethyl acetate costus root extract. Experiments based on cell anti-cancer activity may be one of the most promising targets for novel cancer treatment strategies.

Source link: https://doi.org/10.21786/bbrc/15.1.25


Cytotoxic activity of Cantigi leaf extract (Vaccinium varingiaefolium Blume Miq.) on HeLa cervical cancer cells and A549 lung cancer cells

Cancer treatment often involves multidisciplinary approaches and is uncomfortable. Previous studies revealed that the Cantigi leaf ethyl acetate extract has cytotoxic activity in L1210 leukaemia cells, is good on MCF-7 cells, and T47D cells, but no reports have been published on HeLa and A549 cells. Objective: Determine the cytotoxic activity of the ethyl acetate extract of Cantigi leaf on HeLa cells and A549 cells. Methods: Powdered dry young Cantigi leaves were macerated with hexane and then ethyl acetate. 79. 69. 4 ppm on HeLa cells, the IC50 of the ethyl acetate extract on A549 cells was 75. 74 ppm, but on the HeLa cells, it was 79. 69. 74 ppm. Conclusion: The ethyl acetate extract of Cantigi leaves demonstrated potent in vitro cytotoxic activity on HeLa cervical cancer cells and A549 lung cancer cells.

Source link: https://doi.org/10.46542/pe.2022.222.147150


IC261 inhibits the epithelial-mesenchymal transition induced by TGF-β in A549 lung cancer cells

Abstract Despite rapid advancements in cancer diagnosis and therapy, lung cancer remains to be the leading cause of cancer-related deaths. The expression of transforming growth factor -1-induced mesenchymal cell markers, including N-cadherin, vimentin, and -catenin, was significantly reduced at the mRNA and protein levels in A549 lung cancer cells, which was confirmed by immunofluorescence staining. In addition, IC261 treatment inhibited TGF-induced migration activity in A549 cells and phosphorylation of Smad2 and Smad3.

Source link: https://doi.org/10.1186/s13765-022-00690-1


Abstract 1582: T-SIGn cancer gene therapy and anti-EGFR CAR-T cells synergize in combination therapy to clear A549 lung tumor xenografts and lung metastases in NSG mice

Abstract chimeric antigen receptor T cell therapy is a safe treatment for hematologic malignancies, but solid tumors have demonstrated limited efficacy. Virotherapy, a new emerging cancer treatment that has so far only demonstrated limited clinical benefit as a monotherapy for solid tumors. Importantly, in addition to their ability to specifically kill tumor cells, viral vectors can also be used to “reprogram” the TME from an immunosuppressive to a pro-inflammatory environment. Human lung cancer A549 xenografts were implanted intravenously with the T-SIGn virus and then treated with human anti-EGFR CAR-T cells to prove this hypothesis. In the xenografts of animals treated with combination therapy, transcription optimisation was shown, as well as an increase in transcripts involved in type I IFN responses, as well as a boost in gene expression, T cell activation, and inflammation, which indicated a reprogramming of the TME to more efficiently recruit and/or raise T-cell responses. In addition, the combination therapy reduced the number of A549 tumor cell micrometastases detectable in the lungs by a large number. These findings, taken together, show that combination therapy of a T-SIGn vector and CAR T cells has a lot of promise to be safe in humans with solid tumors. T-SIGn cancer gene therapy and anti-EGFR CAR-T cells collaborate in combination therapy to eliminate A549 lung tumor xenografts and lung metastases in NSG mice [abstract].

Source link: https://doi.org/10.1158/1538-7445.am2021-1582


Abstract 322: Protein expression shift and potential diagnostic markers through proteomics profiling of A549 lung cancer cells

Abstract Highlights: Adenocarcinoma lung cancer is common but difficult to detect. When methanol extract of Calotropis procera was used for the treatment groups, no one is known for its proteome. Adenocarcinoma lung cancer is a common form of lung cancer, but the treatment and diagnosis are challenging. We concentrated on the protein expression of Adenocarcinoma lung cancer cells using A549 cancer cells and introduced new diagnostic techniques and methods in which methanol extracts of Calotropis procera improve the disease. A549 lung cancer cell lines were retrieved, and there are three control groups and three treatment groups. The treatment groups were treated with 80 ug/ml of methanol extracts of Calotropis procera leaf and proteins for tandem mass spectrometry. It also reveals the molecular mechanisms by which the methanol extracts of Calotropis procera leaf prevent carcinogenesis.

Source link: https://doi.org/10.1158/1538-7445.am2021-322


Effect of Kabasura Kudineer Extract on Inhibitory Kappa B Kinase Beta and m TOR mRNA Complex Expression in Lung Cancer Cells (A549 Cell)

Background: Lung cancer has the highest mortality risk and the highest incidence of metastasis. In lung cancer cells, the aim of the research was to determine the effect of kabasura kudineer extract on inhibitory kappa B kinase beta and mTOR mRNA complex expression. B Kinase and mTOR were detected by mRNA expression by real-time PCR. In lung cancer cell lines, the kudineer's inhibition of mRNA expression of inhibitory kappa B Kinase and mTOR has slowed down. Conclusion: According to the report, kabasura kudineer extract has anti-canceral activity on the lung cancer cell line.

Source link: https://doi.org/10.9734/jpri/2021/v33i61a35675


MiR-17-5p/RRM2 Regulated Gemcitabine Resistance in Lung Cancer A549 Cells

MiR-17-5p overexpression in A549/G+ cells increased the number of G1 phase cells and reduced the number of S phase cells in A549/G+ cells, according to Cell cycle analysis; on the other hand, low expression level miR-17-5p gave the opposite results in A549/G- cells. The expression levels of cell cycle related proteins, CCNE1, CCNA2, and P21 decreased in A549/G+ cells, when miR-17-5p was highly expressed, according to the opposite results in A549/G+ cells. PTEN and PI3K were found to be higher in A549/G+ cells, according to a Western blot analysis of signal pathway proteins, but p-PTEN was lower. The level of p-PTEN increased and the level of p-AKT decreased in A549/G+ cells after miR-17-5p overexpressed in A549/G+ cells, and the number of p-AKT decreased; when miR-17-5p expressed low in A549/G-cells, the expression of p-PTEN and p-AKT were reversed; when miR-17-5p expressed low in A549/G+ cells, as miR-17-5p-PTEN p-PTEN increased in p-AKT decreased in A549/G-AKT decreased; during miR-17-5p-AKT-B/G-MG-K-Ct decreased; p-AKT was p-PTEN was reduced in A549/G-cells; p-A549/G-PTEN was low in A549/G-PTEN was unchanged; in A549/G-G-cells; p-PTEN was unchanged in A549/G-A549/G-K-S RRM2 was found to be the target gene for miR-17-5p, according to a dual-luciferase experiment.

Source link: https://doi.org/10.21203/rs.3.rs-1445167/v1


Apoptosis inducing potential of Cyclosporine C in human lung cancer cells (A549)

Cyclotides are a large group of plant-based cyclic peptides that have attracted significant attention in the field of peptide drug design. Cyclosporine C's cytotoxic activity was determined by this research, which included MTT, Hoechst staining, DNA fragmentation, Flowcytometry, and Western blot, which were carried out on a Lung adenocarcinoma cell line A549. The primary aim of this research was to establish Cyclosporine C as a safe novel anticancer drug in the treatment of lung cancer treatment, and to determine the physiological differences caused by Cyclosporine C. We can conclude that Cyclosporine C causes apoptosis in Lung's adenocarcinoma cell line A549. We can infer the information obtained that we can infer the fact that from the study's findings, we can say that Cyclosporine C causes apoptosis.

Source link: https://doi.org/10.25303/1702rjbt1521

* 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