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.

scholarly journals Knockdown of RAD54B expression reduces cell proliferation and induces apoptosis in lung cancer cells

2019 ◽  
Vol 47 (11) ◽  
pp. 5650-5659 ◽  
Author(s):  
Chuan Xu ◽  
Di Liu ◽  
Hong Mei ◽  
Jian Hu ◽  
Meng Luo
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Caspase 3 ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Gene And Protein Expression ◽  
Healthy Lung

Objective RAD54 homolog B (RAD54B), a member of the SNF2/SWI2 superfamily, is implicated in homologous recombination, and high RAD54B expression predicts the prognostic outcomes of lung adenocarcinoma. However, its role in lung carcinogenesis was unclear so this was determined in the present study. Methods We evaluated the gene and protein expression of RAD54B in 15 lung adenocarcinoma tissues and matched adjacent healthy lung tissues by real-time PCR, immunohistochemical staining, and western blotting. A549 lung cancer cells were transduced with lentivirus carrying small hairpin RNA (shRNA) against RAD54B (shRAD54B) or control shRNA (shCtrl), and cell proliferation, viability, apoptosis, and caspase 3/7 activity were evaluated. Results RAD54B protein expression was significantly higher in lung adenocarcinoma tissues than in healthy lung tissues. RAD54B gene expression was high in A549 cells but was efficiently knocked down using shRAD54B with an infection efficiency of 80% and a knockdown ratio of 72.2% compared with shCtrl. Suppressing RAD54B expression in A549 cells significantly reduced cell proliferation and caspase 3/7 activity, and significantly increased the apoptotic rate. Conclusions RAD54B exerts an oncogenic role in lung cancer cell proliferation.

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 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.

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