scholarly journals Effect of taurine on cell proliferation and apoptosis human lung cancer A549 cells

Author(s):  
Shuo Tu ◽  
Xia‑Li Zhang ◽  
Hui‑Fang Wan ◽  
Yan‑Qin Xia ◽  
Zhuo‑Qi Liu ◽  
...  
Lung Cancer ◽  
2019 ◽  
Vol 132 ◽  
pp. 99-106 ◽  
Author(s):  
Jung Ki Yoo ◽  
Ji Min Lee ◽  
Seung Hee Kang ◽  
Seong Ho Jeon ◽  
Chang Min Kim ◽  
...  

2013 ◽  
Vol 437 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Tian Jun Chen ◽  
Fei Gao ◽  
Tian Yang ◽  
Asmitanand Thakur ◽  
Hui Ren ◽  
...  

2021 ◽  
Author(s):  
Jialin Sun ◽  
Zhanqi Cao ◽  
Shiwei Sun ◽  
Zhonghua Sun ◽  
Shuhong Sun ◽  
...  

Abstract Objectives:Our study aimed to evaluate the antitumor effects of 2,2',4'-trihydroxychalcone (7a) on human lung cancer cell line A549. Methods:A549 cells were treated with different concentrations of 7a for different times. The cells without 7a were set as the negative control group. The cell proliferation, invasion, vasculogenic mimicry (VM) formation, heterogeneous adhesion, apoptosis were, respectively, measured by CCK-8, transwell invasion assay, vasculogenic mimicry assay, adhesion assay and flow cytometry. In addition, the expression of related proteins were examined via western blot or ELISA. Results:Our research found that 7a had a significant inhibitory effect on the survival rate of lung cancer A549 cells, while almost had no effect on human lung epithelial BEAS-2B cells and human venous endothelial cells (HUVECs). The migration rate, VM length, invasion and heterogeneous adhesion number of cells treated with 7a significantly decreased as the increase in concentration, while the apoptosis rate increased. Western blot analysis showed that 7a treatment significantly upregulated the expression of E-cadherin, cleaved PARP, Bax, caspase-3, and simultaneously downregulated the expression of MMP-2/9, Bcl-2, p-PI3K, p-Akt, p-MTOR, VEGF, E-selectin and N-cadherin. At the same time, ELISA results found that the pro-angiogenic factor VEGF level in culture media was reduced in the presence of 7a. Additionally, 7a could also reduce the nucleus NF-κB protein level, which would inhibit gene transcription of tumor activity-related proteins. Conclusion:7a might exert inhibitory effects on A549 cells via inhibiting cell proliferation, migration, VM formation, heterogeneous adhesion and inducing apoptosis through suppressing the PI3K/AKT/NF-κB signaling pathway, suggesting that 7a might have therapeutic potential for the treatment of lung cancer.


Author(s):  
Elham Hoveizi ◽  
Fatemeh Fakharzadeh Jahromi

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.


2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Weidong Ma ◽  
Ziyuan Wang ◽  
Yan Zhao ◽  
Qibin Wang ◽  
Yonghong Zhang ◽  
...  

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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