scholarly journals Biodegradable Alginate-Chitosan Hollow Nanospheres for Codelivery of Doxorubicin and Paclitaxel for the Effect of Human Lung Cancer A549 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Liu Tao ◽  
Jie Jiang ◽  
Yu Gao ◽  
Chao Wu ◽  
Ying Liu
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
Hollow Structure ◽  
A549 Cells ◽  
Amorphous State ◽  
Cell Uptake ◽  
Human Lung Cancer ◽  
Scanning Calorimetry ◽  
Adsorption Method ◽  
Multiple Drugs

A biodegradable alginate coated chitosan hollow nanosphere (ACHN) was prepared by a hard template method and used for codelivery of doxorubicin (DOX) and paclitaxel (PTX) to investigate the effect on human lung cancer A549 cells. PTX was loaded into the nanometer hollow structure of ACHN through adsorption method. DOX was coated on surface of ACHN through electrostatic interaction. Drug release studies exhibited a sustained-release effect. According to X-ray diffraction patterns (XRD), differential scanning calorimetry (DSC), and Fourier transform infrared spectroscopy (FT-IR) analysis, DOX structure in the loading samples (DOX-PTX-ACHN) was of amorphous state while PTX was microcrystalline. Cytotoxicity experiments showed ACHN was nontoxic as carrier material and the combination of DOX and PTX in DOX-PTX-ACHN exhibited a good inhibiting effect on cell proliferation. Cell uptake experiments demonstrated that DOX-PTX-ACHN accumulated in the cytoplasm. Degradation experiments illustrated that ACHN was a biodegradable material. In summary, these results clearly indicate that ACHN can be utilized as a potential biomaterial to transport multiple drugs to be used in combination therapy.

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.

scholarly journals Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid inhibits growth of human lung cancer A549 cells by arresting cell cycle and triggering apoptosis

2012 ◽  
Vol 24 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Li Li ◽  
George G. Chen ◽  
Ying-nian Lu ◽  
Yi Liu ◽  
Ke-feng Wu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer

scholarly journals siRNA-mediated MDM2 inhibition sensitizes human lung cancer A549 cells to radiation

2007 ◽  
Author(s):  
Wanfeng Guo ◽  
Kazi Ahmed ◽  
Yanpin Hui ◽  
Guozheng Guo ◽  
Jian Li
Keyword(s):  
Lung Cancer ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer

Sulfated galactofucan from Sargassum thunbergii induces senescence in human lung cancer A549 cells

2020 ◽  
Vol 11 (5) ◽  
pp. 4785-4792
Author(s):  
Yizhong Bao ◽  
Xinyue He ◽  
Wanli Wu ◽  
Sanying Wang ◽  
Jihuan Dai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Human Lung ◽  
A549 Cells ◽  
Cell Senescence ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Sargassum Thunbergii

Our data indicated that a sulfated galactofucan (SWZ-4-H) from Sargassum thunbergii could induce lung cancer cell senescence by regulating p53, p21, p16, and p-Rb.

scholarly journals The inhibition of chloride intracellular channel 1 enhances Ca2+ and reactive oxygen species signaling in A549 human lung cancer cells

2019 ◽  
Vol 51 (7) ◽  
Author(s):  
Jae-Rin Lee ◽  
Jong-Yoon Lee ◽  
Hyun-Ji Kim ◽  
Myong-Joon Hahn ◽  
Jong-Sun Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cancer Cells ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Oxygen Species ◽  
Human Lung Cancer Cells ◽  
Intracellular Ca ◽  
Intracellular Channel

AbstractChloride intracellular channel 1 (CLIC1) is a promising therapeutic target in cancer due to its intrinsic characteristics; it is overexpressed in specific tumor types and its localization changes from cytosolic to surface membrane depending on activities and cell cycle progression. Ca2+ and reactive oxygen species (ROS) are critical signaling molecules that modulate diverse cellular functions, including cell death. In this study, we investigated the function of CLIC1 in Ca2+ and ROS signaling in A549 human lung cancer cells. Depletion of CLIC1 via shRNAs in A549 cells increased DNA double-strand breaks both under control conditions and under treatment with the putative anticancer agent chelerythrine, accompanied by a concomitant increase in the p-JNK level. CLIC1 knockdown greatly increased basal ROS levels, an effect prevented by BAPTA-AM, an intracellular calcium chelator. Intracellular Ca2+ measurements clearly showed that CLIC1 knockdown significantly increased chelerythrine-induced Ca2+ signaling as well as the basal Ca2+ level in A549 cells compared to these levels in control cells. Suppression of extracellular Ca2+ restored the basal Ca2+ level in CLIC1-knockdown A549 cells relative to that in control cells, implying that CLIC1 regulates [Ca2+]i through Ca2+ entry across the plasma membrane. Consistent with this finding, the L-type Ca2+ channel (LTCC) blocker nifedipine reduced the basal Ca2+ level in CLIC1 knockdown cells to that in control cells. Taken together, our results demonstrate that CLIC1 knockdown induces an increase in the intracellular Ca2+ level via LTCC, which then triggers excessive ROS production and consequent JNK activation. Thus, CLIC1 is a key regulator of Ca2+ signaling in the control of cancer cell survival.

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