scholarly journals Mitochondrial DNA mutations are involved in the acquisition of cisplatin resistance in human lung cancer A549 cells

2021 ◽  
Vol 47 (2) ◽  
Author(s):  
Sayo Horibe ◽  
Kaori Ishikawa ◽  
Kazuto Nakada ◽  
Masaki Wake ◽  
Norihiko Takeda ◽  
...  
Mitochondrion ◽  
2007 ◽  
Vol 7 (5) ◽  
pp. 347-353 ◽  
Author(s):  
Xiongjie Jin ◽  
Jianjun Zhang ◽  
Yanning Gao ◽  
Keyue Ding ◽  
Naishu Wang ◽  
...  

2015 ◽  
Vol 36 (3) ◽  
pp. 893-906 ◽  
Author(s):  
Tian-Jun Chen ◽  
Yue-Fei Zhou ◽  
Jie-Juan Ning ◽  
Tian Yang ◽  
Hui Ren ◽  
...  

Background: Drug combination therapies using cisplatin and natural products are common practice in the treatment of human lung cancer. Osthole is a natural compound extracted from a number of medicinal plants and has been shown to exert strong anticancer activities with low toxicity. Methods: In the present study, NBM-T-BMX-OS01 (BMX), derived from the semi-synthesis of osthole, was evaluated in cisplatin treated A549 cells to investigate its effect on cisplatin resistance in human lung cancer. The anticancer effect of BMX were measured by cell viablity‚ colony formation‚ TUNEL staining‚ flow cytometry and cell cycle assay. The fluorescence staining was performed to detect intracellular and mitochondrial reactive oxygen species (ROS) generation. Western blot analysis, antagonists pretreatment and small interfering RNA (siRNA) transfection were used to determine the potential mechanism. Results: It was found that, in comparison with single cisplatin treatment, the combination of BMX and cisplatin resulted in greater efficacy in inhibition of proliferation and colony formation, apoptosis induction and cell cycle arrest. The results of fluorescence staining showed that the combination effect of BMX and cisplatin was due to oxidative stress induced by mitochondrial ROS generation. In addition, BMX significantly attenuated the phosphorylation of ERK and Akt, two important pro-survival kinases. In contrast, BMX inhibited the activation of AMPK, and knockdown of AMPK using specific siRNA partially reversed BMX-induced inhibition of ERK and Akt, as well as its synthetic effects on cisplatin induced anticancer activity in A549 cells. Conclusion: Taken together, this study provides that BMX might modulate cisplatin resistance through AMPK-ERK and AMPK-Akt pathways. These results also support the role of BMX as a potential drug candidate for use in combination with cisplatin in the treatment of human lung cancer.


2018 ◽  
Vol 507 (1-4) ◽  
pp. 426-432 ◽  
Author(s):  
Sayo Horibe ◽  
Shoji Kawauchi ◽  
Toshihito Tanahashi ◽  
Naoto Sasaki ◽  
Shigeto Mizuno ◽  
...  

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.


2012 ◽  
Vol 24 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Li Li ◽  
George G. Chen ◽  
Ying-nian Lu ◽  
Yi Liu ◽  
Ke-feng Wu ◽  
...  

Author(s):  
Wanfeng Guo ◽  
Kazi Ahmed ◽  
Yanpin Hui ◽  
Guozheng Guo ◽  
Jian Li

Sign in / Sign up

Export Citation Format

Share Document