scholarly journals Study of the Effects of Betaine and/or C-Phycocyanin on the Growth of Lung Cancer A549 CellsIn VitroandIn Vivo

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Rea Bingula ◽  
Carmen Dupuis ◽  
Chantal Pichon ◽  
Jean-Yves Berthon ◽  
Marc Filaire ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Combined Treatment ◽  
A549 Cells ◽  
Control Group ◽  
Synergistic Activity ◽  
Daily Food ◽  
M Phase ◽  
A Cell

We investigated the effects of betaine, C-phycocyanin (C-PC), and their combined use on the growth of A549 lung cancer bothin vitroandin vivo.When cells were coincubated with betaine and C-PC, an up to 60% decrease in viability was observed which is significant compared to betaine (50%) or C-PC treatment alone (no decrease). Combined treatment reduced the stimulation of NF-κB expression by TNF-αand increased the amount of the proapoptotic p38 MAPK. Interestingly, combined treatment induced a cell cycle arrest in G2/M phase for ~60% of cells.In vivostudies were performed in pathogen-free male nude rats injected with A549 cells in their right flank. Their daily food was supplemented with either betaine, C-PC, both, or neither. Compared to the control group, tumour weights and volumes were significantly reduced in either betaine- or C-PC-treated groups and no additional decrease was obtained with the combined treatment. This data indicates that C-PC and betaine alone may efficiently inhibit tumour growth in rats. The synergistic activity of betaine and C-PC on A549 cells growth observedin vitroremains to be further confirmedin vivo.The reason behind the nature of their interaction is yet to be sought.

scholarly journals Normobaric hyperoxia inhibits the progression of lung cancer by inducing apoptosis

2018 ◽  
Vol 243 (9) ◽  
pp. 739-748 ◽  
Author(s):  
Sei Won Kim ◽  
In Kyoung Kim ◽  
Jick Hwan Ha ◽  
Chang Dong Yeo ◽  
Hyeon Hui Kang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
A549 Cells ◽  
Migration And Invasion ◽  
Control Group ◽  
Normobaric Hyperoxia ◽  
Human Lung Cells ◽  
Hyperoxia Exposure

Hypoxia is a critical characteristic of solid tumors with respect to cancer cell survival, angiogenesis, and metastasis. Hyperoxic treatment has been attempted to reverse hypoxia by enhancing the amount of dissolved oxygen in the plasma. In this study, we evaluated the effects of normobaric hyperoxia on the progression of lung cancer to determine whether oxygen toxicity can be used in cancer therapy. Following a tail vein injection of the Lewis lung carcinoma cells, C57BL/6J mice were exposed to a 24-h normobaric hyperoxia/normoxia cycle for two weeks. In addition, A549 lung cancer cells were incubated in a normobaric hyperoxia chamber for a 24-h period. As a result, the size and number of tumors in the lung decreased significantly with exposure to normobaric hyperoxia in the mouse model. Cell viability, colony-forming ability, migration, and invasion all decreased significantly in A549 cells exposed to normobaric hyperoxia and the normal control group exposed to normobaric hyperoxia showed no significant damage. Oxidative stress was more prominent with exposure to normobaric hyperoxia in cancer cells. A549 cells exposed to normobaric hyperoxia showed a significantly higher cell apoptosis ratio compared with A549 cells without normobaric hyperoxia exposure and normal human lung cells (BEAS-2B cells). The Bax/Bcl-2 mRNA expression ratio also increased significantly. Changes in the key regulators of apoptosis were similar between in vivo and in vitro conditions. The p-ERK level decreased, while the p-JNK level increased, after normobaric hyperoxia exposure in A549 cells. This study demonstrated the role of normobaric hyperoxia in inhibiting lung cancer. Normal tissue and cells showed no significant hyperoxic damage in our experimental setting. The anti-tumor effect of normobaric hyperoxia may due to the increased reactive oxygen species activity and apoptosis, which is related to the mitogen-activated protein kinase pathway. Impact statement Normobaric hyperoxia (NBO) is a feasible therapy for cancer with a low complication rate. Although NBO may be beneficial in cancer treatment, very few studies have been conducted; thus, the evidence is thin. This is the first study to clearly demonstrate morphological changes in lung cancer with NBO exposure and to investigate the underlying mechanisms both in vivo and in vitro. This study will arouse interest in NBO treatment and promote further research.

Synergism of gambogenic acid with bortezomib induce apoptosis of multiple myeloma.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 8035-8035
Author(s):  
Runzhe Chen ◽  
Hongming Zhang ◽  
Ping Liu ◽  
Xue Wu ◽  
Baoan Chen
Keyword(s):  
Multiple Myeloma ◽  
Combined Treatment ◽  
Parp Cleavage ◽  
Combination Group ◽  
Control Group ◽  
Primary Tumors ◽  
M Phase ◽  
Induced Apoptosis

8035 Background: Multiple myeloma (MM) is one of the most common primary tumors of the bone marrow that accounts for approximately 10% of all hematological cancer. Gambogenic acid (GNA) is one of the natural compound isolated from gamboge and has demonstrated advantages such as a more potent anticancer effect and less systemic toxicity according to early investigations. In this study, we hypothesized that GNA could synergistically potentiate BTZ-induced apoptosis of MM cells and that combining BTZ and GNA may provide a more effective approach to treat MM. Methods: CCK-8 assay, CI isobologram, flow cytometry, western blot, xenograft tumour models, TUNEL and immunochemistry were used in this study to detect to possible mechanisms of apoptosis led by GNA and BTZ in vitro and in vivo. Results: The percentage of MM.1S in G2/M phase after 48h of 4.0nM BTZ, 0.90μM GNA and combination treatment were 31.09±2.16%, 26.68±1.96% and 19.88±1.89% respectively. The percentage of MM.1S in G2/M phase of control group was 17.23±1.65%. The apoptosis rates of MM.1S cells for 48h were 6.57±0.15% in control group, 89.67±5.15% after treatment with 4.0nM BTZ, 97.80±0.81% after treatment with 0.90μM GNA, and 98.9±3.86% after treatment with 4.0nM BTZ plus 0.9μM GNA respectively. All the treatment groups showed a more significant apoptosis rate compared to that of the control group ( p<0.01). MM.1S tumors were implanted in BALB/Ca nu/nu male mice. The tumor weights of GNA and BTZ plus GNA groups decreased significantly when compared with those of control group (p<0.01 and p<0.001, respectively) and the tumor weight of combination group was significantly less than that of BTZ or GNA group (p<0.001). When mice were treated with BTZ combined with GNA, the tumor inhibition rate was 41.94%, whereas those of mice treated with BTZ or GNA alone were 9.68% and 19.35%, respectively. We also found that the combined treatment could induce more markedly increased apoptosis of MM.1S cells via the activation of PARP cleavage, P53, Caspase-3 cleavage and Bax and inhibition of Bcl-2 expression. Conclusions: Our data support that a synergistic antitumor activity exists between BTZ and GNA, and provide a rationale for successful utilization of dual BTZ and GNA in MM chemotherapy in the future.

scholarly journals The cytotoxic effect of Synadenium grantii extract against human lung carcinoma A549 cells and its role in improvement of histopathological and biomarkers changes in Benzo(a)pyrene-induced lung cancer in rats

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 962-971
Author(s):  
Mamdouh Moawad Ali ◽  
Mahmoud Khattab ◽  
Mie Afify Mohamed ◽  
Rania Mohsen Abdelsalam ◽  
Khaled Mahmoud ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Methanolic Extract ◽  
A549 Cells ◽  
Treated Group ◽  
Control Group ◽  
Chemopreventive Agents ◽  
Standard Drug ◽  
Cytotoxicity Activity

Lung cancer is one of the most lethal cancers which is causing up to 3 million deaths annually worldwide. Therefore, management of lung cancer needs searching for new chemopreventive agents. This work was designed to inspect the chemopreventive potential of different extracts prepared from branches and leaves of Synadenium grantii for screening their effects on lung cancer cells (A549), then the most active extract was used for combating lung cancer induced in animal model. The in vitro results showed that, the methanolic extract was the most active extract against A549 cells with a notable cytotoxicity activity (IC50: 4.30±0.44 µg/ml), which was close to the activity of standard drug, doxorubicin (IC50: 3.50±0.40 µg/ml). The results of the in vivo  experiment, revealed that in B(a)P-treated group, aspartate (AST) and alanine (ALT) transaminase activities as well as the levels of urea, creatinine, alpha-fetoprotein (AFP) and Phosphotylinosital 3 Kinase (PI3K) were significantly increased comparing to control group. However, treatment with S. grantii  ameliorated the increase in these parameters in both after- and before-treatment groups comparing with B(a)P-treated group. This improvement in biochemical results were also supported by improving in morphological and histopathological injuries induced by B(a)P, which indicated that methanolic extract of S. grantii  has a chemoprevention effect on lung cancer.

scholarly journals Mechanism of Hydrogen Gas Promoted Apoptosis of Lung Adenocarcinoma A549 cells through XIAP and BIRC3

2020 ◽  
Author(s):  
Yu Zhang ◽  
Gang Chen ◽  
Feng Zhen Yan ◽  
Fei Li Wang ◽  
Chang Dong Wang
Keyword(s):  
Lung Cancer ◽  
Flow Cytometry ◽  
A549 Cells ◽  
Hydrogen Gas ◽  
Control Group ◽  
Logarithmic Phase ◽  
Differential Expressed Genes ◽  
Lung Adenocarcinoma A549

Abstract Background/AIMLung cancer is the most common reason of cancer-related death in worldwide. Hydrogen gas has been found to have effects on a variety of diseases. At present, it is not reported that the effect of hydrogen gas on lung cancer domestic and overseas. Therefore, we designed this experiment to test the differences in the expression of XIAP, BIRC3 and BAX In vivo and in vitro. Materials and methodsA549 cells in logarithmic phase were treated by 20%, 40%, 60% hydrogen gas respectively. Then the apoptosis of different groups were detected by Flow cytometry. We identify the differential expressed genes(DEGs) by transcriptional. The protein expression of XIAP, BIRC3 and BAX were detected by western blot and immunohistochemistry. ResultThe results demonstrated that hydrogen gas can significantly induce apoptosis compared with the control group. The expression of XIAP and BIRC3 were downregulated in hydrogen group. ConclusionHydrogen gas may promote the apoptosis of lung cancer A549 cells by reducing the expression of XIAP and BIRC3 protein.

scholarly journals Effects of Laminaria Japonica Polysaccharides on the Survival of Non-Small-Cell Lung Cancer A549 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Mengxing Yao ◽  
XiaoJun Qian ◽  
Houying Qin
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Control Group ◽  
Small Cell Lung

Objective. To investigate the effect of Laminaria japonica polysaccharides (LJP) on the survival of non-small-cell lung cancer (NSCLC) A549 cells and its mechanism. Methods. In vitro: the cells were randomly divided into control group, LJP (5 mg/ml) group, LJP (10 mg/ml) group, and LJP (20 mg/ml) group. After corresponding treatment, the survival rate and the expression of proteins related to proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and signaling pathway were detected by CCK8 assay and Western blot, respectively. In vivo: a xenograft model was established to detect the tumor volume and mass and the expression of the above pathway proteins. Results. Compared with the control group, LJP decreased the survival rate of A549 cells (P<0.05), inhibited the protein expression of Ki67 and PCNA (P<0.05), downregulated the expression of Bcl-2 while upregulated the expression of Bax, cl-caspase-3, and cl-caspase-9 (P<0.05), upregulated the expression of E-cadherin, downregulated the expression of vascular endothelial growth factor (VEGF) and N-cadherin (P<0.05), and downregulated β-catenin, transcription factor-4 (TCF4), and c-Myc protein expression levels (P<0.05). In vivo: LJP decreased the volume and mass of the xenograft tumors and downregulated β-catenin, TCF4, and c-Myc protein expression levels compared with the control group (P<0.05). Conclusion. LJP can inhibit the survival of non-small-cell lung cancer A549 cells in vitro, and its mechanism is related to the inhibition of activation of β-catenin/TCF4 pathway activation.

scholarly journals α-Hederin inhibits the growth of lung cancer A549 cells in vitro and in vivo by decreasing SIRT6 dependent glycolysis

2020 ◽  
Vol 59 (1) ◽  
pp. 11-20
Author(s):  
Cong Fang ◽  
Yahui Liu ◽  
Lanying Chen ◽  
Yingying Luo ◽  
Yaru Cui ◽  
...  
Keyword(s):  
Lung Cancer ◽  
A549 Cells

scholarly journals Baicalein suppresses vasculogenic mimicry through inhibiting RhoA/ROCK expression in lung cancer A549 cell line

2020 ◽  
Vol 52 (9) ◽  
pp. 1007-1015
Author(s):  
Zhe Zhang ◽  
Li Nong ◽  
Menglei Chen ◽  
Xiaoli Gu ◽  
Weiwei Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Vasculogenic Mimicry ◽  
A549 Cells ◽  
A549 Cell Line ◽  
Traditional Herbal Medicine ◽  
Underlying Mechanisms ◽  
Filament Network ◽  
Lung Cancer A549 Cell

Abstract Vasculogenic mimicry (VM) refers to a new tubular network of the blood supply system with abundant extracellular matrix. VM is similar to capillaries but does not involve endothelial cells. As a traditional herbal medicine commonly used in China, baicalein possesses anti-inflammatory and lipoxygenase activities. However, the effects of baicalein on the process of VM formation in non-small cell lung cancer (NSCLC) and the underlying mechanisms have remained poorly understood. In this study, baicalein was found to inhibit the viability and motility of A549 cells and induced the breakage of the cytoskeletal actin filament network. In addition, baicalein significantly decreased the formation of VM and downregulated the expressions of VM-associated factors, such as VE-cadherin, EphA2, MMP14, MMP2, MMP9, PI3K and LAMC2, similar to the effects of ROCK inhibitors. Indeed, baicalein inhibited RhoA/ROCK expression in vitro and in vivo, suggesting the underlying mechanisms of reduced VM formation. Collectively, baicalein suppressed the formation of VM in NSCLC by targeting the RhoA/ROCK signaling pathway, indicating that baicalein might serve as an emerging drug for NSCLC.

scholarly journals Molecular Role of EGFR-MAPK Pathway in Patchouli Alcohol-Induced Apoptosis and Cell Cycle Arrest on A549 CellsIn VitroandIn Vivo

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
XinGang Lu ◽  
Liu Yang ◽  
ChengHua Lu ◽  
ZhenYu Xu ◽  
HongFu Qiu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mapk Pathway ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Activity Measurement ◽  
Cover Glass ◽  
Patchouli Alcohol ◽  
Pogostemon Cablin

Nowadays, chemotherapy is still the main effective treatment for cancer. Herb prescriptions containingPogostemon cablin Benth(also known as “Guang-Huo-Xiang”) have been widely used in Chinese medicine today. In our research, we found that patchouli alcohol, a compound isolated from the oil ofPogostemon cablin Benth, exerted antitumor ability against human lung cancer A549 cells ability bothin vitroandin vivo. MTT assay was used to assess cell viability. Hoechst 33342 staining and TUNEL cover glass staining provided the visual evidence of apoptosis. Caspase activity measurement showed that patchouli alcohol activated caspase 9 and caspase 3 of mitochondria-mediated apoptosis. Consistently, patchouli alcohol inhibited the xenograft tumorin vivo. Further investigation of the underlying molecular mechanism showed that MAPK and EGFR pathway might contribute to the antitumor effect of patchouli alcohol. Our study proved that patchouli alcohol might be able to serve as a novel antitumor compound in the clinical treatment of lung cancer.

scholarly journals Dendrobine Inhibits γ-Irradiation-Induced Cancer Cell Migration, Invasion and Metastasis in Non-Small Cell Lung Cancer Cells

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 954
Author(s):  
Ye-Ram Kim ◽  
Ah-Reum Han ◽  
Jin-Baek Kim ◽  
Chan-Hun Jung
Keyword(s):  
Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Migration And Invasion ◽  
Inhibitory Effects ◽  
Invasion And Metastasis ◽  
Small Cell Lung ◽  
Γ Irradiation

The use of ionizing radiation (IR) during radiotherapy can induce malignant effects, such as metastasis, which contribute to poor prognoses in lung cancer patients. Here, we explored the ability of dendrobine, a plant-derived alkaloid from Dendrobium nobile, to improve the efficacy of radiotherapy in non-small cell lung cancer (NSCLC). We employed Western blotting, quantitative real-time (qRT)-PCR, transwell migration assays, and wound-healing assays to determine the effects of dendrobine on the migration and invasion of A549 lung cancer cells in vitro. Dendrobine (5 mm) inhibited γ-irradiation-induced migration and invasion of A549 cells by suppressing sulfatase2 (SULF2) expression, thus inhibiting IR-induced signaling. To investigate the inhibitory effects of dendrobine in vivo, we established a mouse model of IR-induced metastasis by injecting BALB/c nude mice with γ-irradiated A549 cells via the tail vein. As expected, injection with γ-irradiated cells increased the number of pulmonary metastatic nodules in mice (0 Gy/DPBS, 9.8 ± 1.77; 2 Gy/DPBS, 20.87 ± 1.42), which was significantly reduced with dendrobine treatment (2 Gy/Dendrobine, 10.87 ± 0.71), by prevention of IR-induced signaling. Together, these findings demonstrate that dendrobine exerts inhibitory effects against γ-irradiation-induced invasion and metastasis in NSCLC cells in vitro and in vivo at non cytotoxic concentrations. Thus, dendrobine could serve as a therapeutic enhancer to overcome the malignant effects of radiation therapy in patients with NSCLC.

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