scholarly journals Interferon Regulatory Factor-1 Regulates Cisplatin-Induced Apoptosis and Autophagy in A549 Lung Cancer Cells

2021 ◽  
Author(s):  
lemeng zhang ◽  
Tianli Cheng ◽  
Hua Yang ◽  
Jianhua Chen ◽  
Xiaoping Wen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Interferon Regulatory Factor ◽  
Atp Depletion ◽  
Lung Cancer Cells ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 1 ◽  
A549 Lung

Abstract Purpose: This study aimed to investigate the expression and function of interferon regulatory factor-1 (IRF-1) in non-small cell lung cancer (NSCLC). Methods: IRF-1 expression and its prognostic value were investigated through bioinformatic analysis. The protein expression levels of IRF-1, cleaved caspase-3, and LC3-I/II were analyzed by western blotting. A lentiviral vector was used to overexpress or knockdown IRF-1 in vitro. Mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were analyzed by JC-1 and DCFH-DA staining, respectively. ATP, SOD, MDA, cell viability, LDH release, and caspase-3 activity were evaluated using commercial kits. Results: Compared to the levels in normal tissues, IRF-1 expression was significantly lower in lung cancer tissues and was a prognostic factor for NSCLC. Cisplatin treatment induced IRF-1 activation, ROS production, ATP depletion, SOD consumption, and MDA accumulation in A549 lung cancer cells. IRF-1 overexpression promoted mitochondrial depolarization, oxidative stress, and apoptotic cell death and inhibited autophagy in A549 cells, and these effects could be reversed by IRF-1 knockdown. Conclusion: These data suggest that IRF-1 regulates apoptosis, autophagy and oxidative stress, which might be served as a potential target for increasing chemotherapy sensitivity of lung cancer.

scholarly journals Myrcene Exhibits Antitumor Activity Against Lung Cancer Cells by Inducing Oxidative Stress and Apoptosis Mechanisms

2020 ◽  
Vol 15 (9) ◽  
pp. 1934578X2096118
Author(s):  
Xudong Bai ◽  
Jin Tang
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Metabolic Activity ◽  
Lung Cancer Cells ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
A549 Lung

Myrcene, a natural olefinic hydrocarbon, possesses anti-inflammatory, analgesic, antibiotic, and antimutagenic properties, but its anticancer effect has not yet been elucidated. Hence, the present study was framed to investigate the molecular mechanism by which myrcene mediates the anticancer activity of A549 lung adenocarcinoma cells. In vitro, A549 lung cancer cells were cultured either with or without myrcene, and the effects on cellular metabolic activity, levels of reactive oxygen species (ROS), mitochondrial integrity, deoxyribonucleic acid (DNA) damage, and activity of caspases were analyzed. The study demonstrated that compared with control cells, myrcene induces cell death in a dose-dependent manner while inducing ROS levels. Further experiments revealed that the metabolic activity of the A549 lung adenocarcinoma cells was diminished with increased DNA damage and altered cellular integrity. In addition, increased activity of caspase-3 was also evidenced with reduced mitochondrial membrane potential synthesis in the myrcene-treated cells, which demonstrate that lung cancer cells experience signs of toxicity during myrcene treatment through the activation of the apoptosis mechanism via mitochondria-mediated cell death signaling and induction of oxidative stress. The results provide the first report on the evidence of anticancer activity and the possibility of a new drug that could be used for the treatment of lung cancer.

Chemotherapeutic paclitaxel and cisplatin differentially induce pyroptosis in A549 lung cancer cells via caspase-3/GSDME activation

APOPTOSIS ◽  
2019 ◽  
Vol 24 (3-4) ◽  
pp. 312-325 ◽  
Author(s):  
Cheng-cheng Zhang ◽  
Chen-guang Li ◽  
Yao-feng Wang ◽  
Li-hui Xu ◽  
Xian-hui He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Lung Cancer Cells ◽  
A549 Lung

scholarly journals F10, a novel hydatidiform mole-associated gene, inhibits the paclitaxel sensitivity of A549 lung cancer cells by downregulating BAX and caspase-3

2017 ◽  
Vol 13 (4) ◽  
pp. 2563-2568 ◽  
Author(s):  
Yali Song ◽  
Wei Cao ◽  
Xi Zhu ◽  
Zhuolin Qiu ◽  
Xiaoping Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Hydatidiform Mole ◽  
Lung Cancer Cells ◽  
A549 Lung

scholarly journals Anticancer effect of salidroside on A549 lung cancer cells through inhibition of oxidative stress and phospho-p38 expression

2014 ◽  
Vol 7 (4) ◽  
pp. 1159-1164 ◽  
Author(s):  
JUN WANG ◽  
JIAN-ZHE LI ◽  
AI-XIA LU ◽  
KE-FEN ZHANG ◽  
BAO-JIANG LI
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Anticancer Effect ◽  
A549 Lung

scholarly journals Indomethacin-Enhanced Anticancer Effect of Arsenic Trioxide in A549 Cell Line: Involvement of Apoptosis and Phospho-ERK and p38 MAPK Pathways

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Ali Mandegary ◽  
Maryam Torshabi ◽  
Mohammad Seyedabadi ◽  
Bagher Amirheidari ◽  
Elham Sharif ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Cytotoxic Effect ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Lung Cancer Cells ◽  
Gene And Protein Expression ◽  
A549 Lung

Background. Focusing on novel drug combinations that target different pathways especially apoptosis and MAPK could be a rationale for combination therapy in successful treatment of lung cancer. Concurrent use of cyclooxygenase (COX) inhibitors with arsenic trioxide (ATO) might be a possible treatment option.Methods. Cytotoxicity of ATO, dexamethasone (Dex), celecoxib (Cel), and Indomethacin (Indo) individually or in combination was determined at 24, 48, and 72 hrs in A549 lung cancer cells. The COX-2 gene and protein expression, MAPK pathway proteins, and caspase-3 activity were studied for the most cytotoxic combinations.Results. The IC50s of ATO and Indo were 68.7 μmol/L and 396.5 μmol/L, respectively. Treatment of cells with combinations of clinically relevant concentrations of ATO and Indo resulted in greater growth inhibition and apoptosis induction than did either agent alone. Caspase-3 activity was considerably high in the presence of ATO and Indo but showed no difference in single or combination use. Phosphorylation of p38 and ERK1/2 was remarkable in the concurrent presence of both drugs.Conclusions. Combination therapy with ATO and Indo exerted a very potent in vitro cytotoxic effect against A549 lung cancer cells. Activation of ERK and p38 pathways might be the mechanism of higher cytotoxic effect of ATO-Indo combination.

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