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A549 Lung cancer Cells - Europe PMC

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Last Updated: 23 April 2022

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c-Met specific CAR-T cells as a targeted therapy for non-small cell lung cancer cell A549.

Non-small cell lung cancer is one of the most common and fatal malignancies, with a low survival rate. One of the most promising Cellular immunotherapy research fields is Chimeric antigen receptor T cell therapy. Hence, CAR-T cells that target c-Met have been created for use in NSCLC therapy, and may be a potential therapeutic tactic. To obtain the second generation c-Met CAR-T expressing CARs stably, using a lentiviral vector to load the c-Met CAR gene and transfected the c-Met CAR gene into human T cells. In LDH production assay, c-Met CAR-T cells showed particular cellular cytotoxicity in LDH-mediated cytotoxicity in LDH release assay. c-Met positive NSCLC tissue, tissue type, fluorescence intensity, and immunohistochemical analysis demonstrated a larger tumor growth suppression in comparison to untransduced T cells, leading to greater tumor growth suppression in c-Met CAR-T cells. HE staining revealed that c-Met CAR-T cells did not cause side effects in nude mice.

Source link: https://europepmc.org/article/MED/35378051


Salvianolic acid B acts against non‑small cell lung cancer A549 cells via inactivation of the MAPK and Smad2/3 signaling pathways.

Salvianolic acid B is a potent cytotoxic polyphenol against cancer. In the non-small cell lung cancer A549 cell line, the effect of Sal B and its molecular mechanism were investigated in the present study. Sal B inhibited TGF-1-induced EMT and migration of A549 cells, hampered cell cycle progression, and triggered cell autophagy and apoptosis, according to the study. Overall, these findings showed that Sal B may have a potential therapeutic effect against NSCLC in vitro. Sal B's underlying active mechanism, according to the present study's findings, may be closely related to the inhibition of the MAPK and Smad2/3 signaling pathways' inability. Sal B may therefore be a potential candidate NSCLC therapeutic agent.

Source link: https://europepmc.org/article/MED/35348194


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

miR-17-5p's overexpression increased the number of G1 phase cells and reduced the number of S phase cells in A549/G+ cells, reducing the number of S phase cells in A549/G+ cells, according to Cell cycle results; on the other hand, low expression level of miR-17-5p gave the opposite results in A549/G+ cells. When miR-17-5p was highly expressed, cell cycle related proteins, CCNE1, CCNA2, and P21 decreased in A549/G+ cells, according to the same results in A549/G+ cells; in contrast, inhibition of miR-17-5p expression resulted in the opposite results. PTEN and PI3K were expressed higher in A549/G+ cells, according to the Western blot analysis of signal pathway proteins, but p-PTEN were lower in A549/G+ cells. Following miR-17-5p overexpressed in A549/G+ cells, the level of p-PTEN increased and p-AKT decreased, and p-AKT decreased; when miR-17-5p was low in A549/G-cells, the expression of p-PTEN and p-AKT were different; when miR-17-5p expressed low in A549/G-cells; when miR-17-5p expressed low in A549/G-PTEN increased in A549/G-PTEN p-G-PTEN and p-PTEN increased and p-PTEN increased and t decreased; p-AKT decreased; when miR-17-5p-T was unchanged in A549/G-cells, the expression of p-PTEN was reduced in A549/G-PTEN was unchanged in A549/G-CaT was in A549/G-AKT was unchanged in A549/G-G-A549/G+ cells;.

Source link: https://europepmc.org/article/PPR/PPR469676


Gallic Acid Hindered Lung Cancer Progression by Inducing Cell Cycle Arrest and Apoptosis in A549 Lung Cancer Cells via PI3K/Akt Pathway.

This report establishes gallic acid's anti-cancer activity as a promising therapeutic agent with the ability of regulating the PI3K/Akt pathway. TUNEL assay, xenograft mouse model, and histological studies were used to demonstrate our research's accuracy. We used various experimental techniques, including cell viability assay, colony formation assay, tumor spheroid formation assay, TUNEL assay, TUNEL assay, TUNEL assay, Western blot analysis, xenograft mouse model, and histological analysis to demonstrate our findings' validity. Treatment with GA stifled cell proliferation in a dose-dependent manner as shown by cell viability assay at 48 h. GA and cisplatin also stifled colony formation and tumor spheroid formation. In an A549-derived tumor xenograft model, Intraperitoneal injection with GA for four weeks reduced the size of tumor mass, according to the researchers. These findings combined showed that GA slowed lung cancer progression by inducing cell cycle arrest and apoptosis, indicating that GA may be a potential therapeutic agent against non-small cell lung cancer.

Source link: https://europepmc.org/article/MED/34261818


Wasp venom peptide improves the proapoptotic activity of alendronate sodium in A549 lung cancer cells.

Background Lung cancer in both men and women is thought to be the leading cause of cancer-related mortality worldwide. Anti-cancer peptides are a potential untapped source of therapeutic cancer therapy. Using Design-Expert software, a box-Behnken response surface layout was used for the manufacture of Alendronate sodium -mastoparan peptide nanoconjugates. Compared to ALS-Raw, the novel ALS-MP produced the lowest IC50 in comparison to ALS-Raw. Following the treatment with optimized ALS-MP nanoconjugates, cell cycle analysis revealed a significantly higher percentage of cells in the G2-M phase.

Source link: https://europepmc.org/article/MED/35202419


Cinobufagin induces FOXO1-regulated apoptosis, proliferation, migration, and invasion by inhibiting G9a in non-small-cell lung cancer A549 cells.

Bufonis, an animal drug marketed in China, is the product of Bufo gargarizans Cantor or B. melanostictus Schneider's mystery. Aim of the study The aim of the study was to identify the effects of CNB on non-small-cell lung cancer and identify potential molecular mechanisms. Similarly, the amounts of proliferating cell nuclear antigen, cytokeratin8, poly ADP-ribose polymerase, Caspase8, B-cell lymphoma, and mitochondrial N-lysine N-methyltransferase2 in A549 cells were determined using qRT-PCR and/or Western blot analysis, Co-IP, immunofluorescence, and immunohistochemistry were determined using qRT-cytokerat CNB suppressed cell proliferation, migration, and invasion, but A549 cells were promoted apoptosis in a dose- and time-dependent manner, though cinobufagin had no cytotoxic effect on BEAS-2B cells. Since FOXO1 was successfully silenced, CNB did not reverse the changes in the proliferation, migration, invasion, and apoptosis of A549 cells in A549 cells. Conclusions In vitro and in vitro, our research shows that cinobufagin suppresses NSCLC cells' malignant biological behaviours in vivo and in vitro, and that, in vivo and in vitro, this effect may be induced mechanistically, this effect may be achieved by inhibiting the expression of the tumor suppressor gene FOXO1. Our results, taken together, reveal key insights into the molecular mechanisms underlying cinobufagin's anticancer activity, suggesting that cinobufagin's anticancer therapy may be a candidate for targeted cancer therapy.

Source link: https://europepmc.org/article/MED/35176466


Effects of 2,2',4'-trihydroxychalcone on the proliferation, metastasis and apoptosis of A549 human lung cancer cells.

On the A549 human lung cancer cell line, the aim of the present research was to determine the antitumor effects of 2,2',4'-trihydroxychalcone. The present report found that 7a had a significant inhibitory effect on the survival of the A549 lung cancer cells but not so much on BEAS-2B human lung epithelial cells or human venous endothelial cells. The migration rate, VM length, invasion rate, and heterogeneous adhesion number of cells treated with 7a significantly decreased as the concentration increased, though the apoptosis rate increased. The expression levels of metalloproteinase-2/9, p-AKT, cleaved polymerase, Bax, and caspase-3, as well as reduced the expression levels of metalloproteinase-2/9, p-MTOR, vascular endothelial growth factor, E-selectin, and N-cadherin were found to rise after 7a therapy significantly raised the expression levels of E-cadherin In addition, 7a may also reduce the nuclear NF-B protein expression, potentially inhibiting tumor apoptosis and metastasis-related genes.

Source link: https://europepmc.org/article/MED/35261630


Pharmacodynamics and Cellular Uptake of Peimine and Peiminine in Inflammatory Model Non-Small-Cell Lung Cancer Epithelial Cells (A549).

Peimine and peiminine concentrations in A549 cells were determined simultaneously by a rapid and sensitive ultra-performance liquid chromatography-tandem mass spectrometry device. According to peimine and peiminine, the RSDs of intraday and interday precision and accuracy were less than 6. 7 percent and 3. 7 percent, respectively. The combination group had an elevated uptake and had a longer T max than the single group. Peimine and peiminine cell lines' cell lines were tested in A549 cell lines, revealing their cellular uptake characteristics and pharmacokinetics. This research, for the first time, investigates peimine and peiminine's cellular uptake profiles and pharmacodynamics.

Source link: https://europepmc.org/article/MED/35178100


Particulate matter (PM 10 ) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells.

We investigated the role of PM 10 in SETD2's expression and protein levels, as well as the effect on the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis using the A549 lung cancer cell line. In A549 cells, we found that PM 10 decreases the expression and protein levels of SETD2, TUBULIN, and BUBUBR1, as well as increasing the levels of AURORA B and SURVIVIVIN. Compared to untreated cells, we discovered that PM 10 decreased the expression and protein levels of SETD2, -TUBULIN and BUBULIN, and BUBR1 and BUBULIN, as well as the presence of AURORORORA B and protein FIA549 cells, compared to non-treated cells'st HIMZZ, TUBULIN and BUBUBUBUBUBUBUBUBUBULIN and protein AURORA B and protein AURORORA B and SURVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIVIN and protein levels of BUBULIN and protein A549 cells. When compared to the control group, PM 10 also led to a decrease in the mitotic index and the percentage of cells in G2/M. In comparison to non-treated cells, co-localization of SETD2/-TUB was reduced in PM10-treated cells. In contrast to non-treated cells, micronuclei number was higher in PM10-treated cells, and whole chromosomes were more prevalent in PM 10 -treated MN than in non-treated MN.

Source link: https://europepmc.org/article/MED/35134396


ZBM-H-induced activation of GRP78 ATPase promotes apoptosis via annexin A7 in A549 lung cancer cells.

Hypochlorous acid, a hypochlorous acid, is a key signal for the regulation of cancer cell fate, including autophagy and apoptosis. However, the mechanism of cell apoptosis has not been uncovered by GRP78 ATPase. Following ZBM-H treatment, the interaction between GRP78 and the annexin A7 was promoted, and this was followed by increased phosphorylation of integrin44. These results, together, provide new insight into the mechanism by which ZBM-H-induced activation of GRP78 ATPase regulates apoptosis of A549 lung cancer cells.

Source link: https://europepmc.org/article/MED/35118704

* 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