scholarly journals The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

2019 ◽  
Vol 30 (3) ◽  
pp. 197-207 ◽  
Author(s):  
Ibraheem M. Attafi ◽  
Saleh A. Bakheet ◽  
Hesham M. Korashy
Keyword(s):  
Lung Cancer ◽  
Transcription Factors ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Toxicity ◽  
Human Lung Cancer

scholarly journals Epigallocatechin-3-Gallate Enhances the Therapeutic Effects of Leptomycin B on Human Lung Cancer A549 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Meghan M. Cromie ◽  
Weimin Gao
Keyword(s):  
Lung Cancer ◽  
Molecular Mechanisms ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Cancer Drug ◽  
Therapeutic Effects ◽  
Leptomycin B ◽  
Egcg Treatment

Our previous studies have shown Leptomycin B (LMB) is a promising antilung cancer drug. Epigallocatechin-3-gallate (EGCG) has antitumor properties but a debatable clinical application. The objective of this study is to evaluate the combination therapeutic effect of LMB and EGCG and its molecular mechanisms in human lung cancer A549 cells. Increased cytotoxicity was observed in LMB+EGCG-treated cells compared to LMB-treated cells. Elevated ROS was maximized 2 h after treatment, and LMB+EGCG-treated cells had higher ROS levels compared to LMB. N-Acetyl-L-cysteine (NAC) studies confirmed the oxidative role of LMB and/or EGCG treatment. In comparison to the control, CYP3A4, SOD, GPX1, and p21 mRNA expression levels were increased 7.1-, 2.0-, 4.6-, and 13.1-fold in LMB-treated cells, respectively, while survivin was decreased 42.6-fold. Additionally, these increases of CYP3A4, SOD, and GPX1 were significantly reduced, while p21 was significantly increased in LMB+EGCG-treated cells compared to LMB-treated cells. The qRT-PCR results for p21 and survivin were further confirmed by Western blot. Our study first shows that LMB produces ROS and is possibly metabolized by CYP3A4, GPX1, and SOD in A549 cells, and combination treatment of LMB and EGCG augments LMB-induced cytotoxicity through enhanced ROS production and the modulation of drug metabolism and p21/survivin pathways.

scholarly journals The Role of CHMP4C on Proliferation in the Human Lung Cancer A549 Cells

2015 ◽  
Vol 06 (15) ◽  
pp. 1223-1228 ◽  
Author(s):  
Kang Li ◽  
Jianxiang Liu ◽  
Mei Tian ◽  
Chunnan Piao ◽  
Jianlei Ruan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer

scholarly journals Ursolic and Oleanolic Acids Induce Mitophagy in A549 Human Lung Cancer Cells

Molecules ◽  
2019 ◽  
Vol 24 (19) ◽  
pp. 3444 ◽  
Author(s):  
Nayeli Shantal Castrejón-Jiménez ◽  
Kahiry Leyva-Paredes ◽  
Shantal Lizbeth Baltierra-Uribe ◽  
Juan Castillo-Cruz ◽  
Marcia Campillo-Navarro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Oleanolic Acid ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

Ursolic and oleanolic acids are natural isomeric triterpenes known for their anticancer activity. Here, we investigated the effect of triterpenes on the viability of A549 human lung cancer cells and the role of autophagy in their activity. The induction of autophagy, the mitochondrial changes and signaling pathway stimulated by triterpenes were systematically explored by confocal microscopy and western blotting. Ursolic and oleanolic acids induce autophagy in A549 cells. Ursolic acid activates AKT/mTOR pathways and oleanolic acid triggers a pathway independent on AKT. Both acids promote many mitochondrial changes, suggesting that mitochondria are targets of autophagy in a process known as mitophagy. The PINK1/Parkin axis is a pathway usually associated with mitophagy, however, the mitophagy induced by ursolic or oleanolic acid is just dependent on PINK1. Moreover, both acids induce an ROS production. The blockage of autophagy with wortmannin is responsible for a decrease of mitochondrial membrane potential (Δψ) and cell death. The wortmannin treatment causes an over-increase of p62 and Nrf2 proteins promote a detoxifying effect to rescue cells from the death conducted by ROS. In conclusion, the mitophagy and p62 protein play an important function as a survival mechanism in A549 cells and could be target to therapeutic control.

scholarly journals Cisplatin-induced hydroxyl radicals mediate pro-survival autophagy in human lung cancer H460 cells

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Somruethai Sumkhemthong ◽  
Eakachai Prompetchara ◽  
Pithi Chanvorachote ◽  
Chatchai Chaotham
Keyword(s):  
Lung Cancer ◽  
Hydroxyl Radicals ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Radical Scavenger ◽  
Apoptosis Resistance ◽  
Lung Cancer Patients ◽  
Human Lung Cancer Cells ◽  
H460 Cells

Abstract Background Accumulated evidence demonstrates cisplatin, a recommended chemotherapy, modulating pro-survival autophagic response that contributes to treatment failure in lung cancer patients. However, distinct mechanisms involved in cisplatin-induced autophagy in human lung cancer cells are still unclear. Results Herein, role of autophagy in cisplatin resistance was indicated by a decreased cell viability and increased apoptosis in lung cancer H460 cells pre-incubated with wortmannin, an autophagy inhibitor, prior to treatment with 50 µM cisplatin for 24 h. The elevated level of hydroxyl radicals detected via flow-cytometry corresponded to autophagic response, as evidenced by the formation of autophagosomes and autolysosomes in cisplatin-treated cells. Interestingly, apoptosis resistance, autophagosome formation, and the alteration of the autophagic markers, LC3-II/LC3-I and p62, as well as autophagy-regulating proteins Atg7 and Atg3, induced by cisplatin was abrogated by pretreatment of H460 cells with deferoxamine, a specific hydroxyl radical scavenger. The modulations in autophagic response were also indicated in the cells treated with hydroxyl radicals generated via Fenton reaction, and likewise inhibited by pretreatment with deferoxamine. Conclusions In summary, the possible role of hydroxyl radicals as a key mediator in the autophagic response to cisplatin treatment, which was firstly revealed in this study would benefit for the further development of novel therapies for lung cancer.

Proteomic and redox-proteomic study on the role of glutathione reductase in human lung cancer cells

2013 ◽  
Vol 34 (24) ◽  
pp. 3305-3314 ◽  
Author(s):  
Chiao-Yuan Fan ◽  
Hsiu-Chuan Chou ◽  
Yi-Wen Lo ◽  
Yueh-Feng Wen ◽  
Yi-Chih Tsai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Glutathione Reductase ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Proteomic Study

scholarly journals Cytotoxic Effects of Flubendazole in Human Lung Cancer Cell Line A549

2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Elham Hoveizi ◽  
Fatemeh Fakharzadeh Jahromi
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Human Lung ◽  
A549 Cells ◽  
Beclin 1 ◽  
Human Lung Cancer ◽  
Pcr Analysis ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Acridine Orange Staining

Background: The development of effective anticancer drugs is a significant health issue. Previous studies showed that members of the benzimidazole family have anticancer effects on several cancers Objectives: The present study investigated the cytotoxic effect of flubendazole on A549 human lung cancer cells. Methods: The A549 cells were treated with flubendazole at 1, 2, 5, and 10 µM concentrations for three days. Cell viability was measured by the MTT assay and Acridine orange staining. Also, the expressions of P62 and Beclin -1 were analyzed by qRT-PCR analysis. Results: Cell viability of A549 cells, in a concentration-dependent manner, showed significant differences between the treatment and control groups, and the IC50 value was determined to be 2 µM. Also, flubendazole reduced the expression of P62 and increased the expression of Beclin 1 in treated cells. Conclusions: Flubendazole induces cell death in A549 cells in a dose and time-dependent manner and can offer new factors in lung cancer therapeutic strategies.

scholarly journals Salidroside Suppresses the Proliferation and Migration of Human Lung Cancer Cells through AMPK-Dependent NLRP3 Inflammasome Regulation

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Weidong Ma ◽  
Ziyuan Wang ◽  
Yan Zhao ◽  
Qibin Wang ◽  
Yonghong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Nlrp3 Inflammasome ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Human Lung Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

Inflammatory reactions mediated by the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome contributes to non-small-cell lung cancer (NSCLC) progression, particularly in patients with bacterial infections. Salidroside (SAL) has recently been shown to suppress lipopolysaccharide- (LPS-) induced NSCLC proliferation and migration, but its mechanism of action remains unclear. It has been shown that SAL improves metabolic inflammation in diabetic rodents through AMP-activated protein kinase- (AMPK-) dependent inhibition of the NLRP3 inflammasome. However, whether the NLRP3 inflammasome is regulated by SAL in NSCLC cells and how its underlying mechanism(s) can be determined require clarification. In this study, human lung alveolar basal carcinoma epithelial (A549) cells were treated with LPS, and the effects of SAL on cell proliferation, migration, AMPK activity, reactive oxygen species (ROS) production, and NLRP3 inflammasome activation were investigated. We found that LPS induction increases the proliferation and migration of A549 cells which was suppressed by SAL. Moreover, SAL protected A549 cells against LPS-induced AMPK inhibition, ROS production, and NLRP3 inflammasome activation. Blocking AMPK using Compound C almost completely suppressed the beneficial effects of SAL. In summary, these results indicate that SAL suppresses the proliferation and migration of human lung cancer cells through AMPK-dependent NLRP3 inflammasome regulation.

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