scholarly journals Investigating Cytotoxic Effects and Molecular Mechanisms of Quinoa Seed Extract Against Human Lung Cancer Cell Lines

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Homa Mollaei ◽  
Farzaneh Karimi ◽  
Morteza Ghorbany ◽  
Mahboubeh Sadat Hosseinzadeh ◽  
Maryam Moudi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
A549 Cells ◽  
Seed Extract ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Expression Levels ◽  
Seed Extracts

Background: Lung cancer is one of the most common leading causes of mortality and morbidity worldwide. Despite recent advances in therapeutic approaches, common methods are not fully effective. Thus, researchers are looking for some novel complementary agents to improve the effectiveness of therapies. Emerging evidence has shown the antitumor activity of several natural components such as quinoa seed extracts in various types of cancer. Objectives: Hence, this study was conducted to evaluate the antiproliferation and anti-apoptotic activity of quinoa on the A549 lung cancer cell line. Methods: The cell viability of A549 cells treated with quinoa was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of BAX and BCL2 as apoptosis-related genes were assessed using real-time polymerase chain reaction (PCR). Finally, the statistical analysis was performed using GraphPad Prism version 7. Results: Our findings demonstrated that the cell viability decreased in a concentration and time-dependent manner. Also, treating A549 cells with doses of 1.60 and 1.92 mg/mL of quinoa seed extracts could increase BAX and decrease BCL2 expression levels (P < 0.05). However, the higher dose (1.92 mg/mL) was significantly effective. Conclusions: According to this study, quinoa seed extract could induce apoptosis in lung cancer cells (A549) throughout the increased ratio of BAX/BCL2. However, further investigations are required to confirm the results.

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 Effect of Kabasura Kudineer Extract on Inflammatory Cytokines [Interleukin-6 and Tumour Necrosis Factor-α] in Lung Cancer Cell Line A549

2021 ◽  
pp. 653-660
Author(s):  
M. Afrin Nisha ◽  
S. Preetha ◽  
J. Selvaraj ◽  
G. Sridevi
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
Inflammatory Cytokines ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Tnf Α

Background: Kabasura kudineer is widely known for its anticancer efficiency. Kabasura kudineer is a customary formulation used by siddha practitioners for effectively managing common respiratory illness. Herbal medicines are acknowledged as a great approach to lung cancer therapy. Aim of the study is to know about the anticancer property of Kabasura kudineer extract on inflammatory cytokines IL-6 and TNF-α in lung cancer cell line (A549). Materials and Methods: Human lung cancer cell line (A549) was purchased from National Centre for Cell Sciences (NCCS), Pune, India. Cell viability test was done by MTT assay. Gene expression analysis was done by Real Time-PCR. The obtained data were analysed statistically by one-way analysis of variance and Duncan’s multiple range test with Graph Pad Prism version 5 to analyse the significance. The significance was considered at p<0.05 level in Duncan’s test. Results and Discussion: Kabasura kudineer caused a marked increase in cell death in dose dependent manner. AT the end of 48 hours, maximum inhibition was at 400 and 500 μg/ml. Kabasura kudineer extract reduced the expression of IL-6 and TNF-α compared to the control cells. Conclusion: This study concluded that Kabasura kudineer extract has anticancer activity on lung cancer cell lines (A549).

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 Cytotoxicity effect of ethanolic extract of Mikania glomerata against A549 human lung cancer cell line

2016 ◽  
Vol 2 (7) ◽  
pp. 139 ◽  
Author(s):  
S. Sarojini ◽  
V. Ramesh ◽  
P. Senthilkumaar
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cell Line ◽  
Cancer Cell ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Mikania Glomerata

The genus Mikania is the largest of its kind in the family Eupatorieae (Asteraceae), with more than 430 species concentrated mainly in the tropical regions, among which, Mikania glomerata is a most common herb generally employed in the treatment of respiratory disorders. The Milania glomerata plant leaf extracts were used for anticancer study against A549 human lung cancer cell line. The solid liquid extraction method has been employed to prepare the ethanol extract of Mikania glomerata through soxhelt apparatus method. To check the anti-proliferative effect of this extract, the extract chosen was tested for cell viability on the lung cancer cells A549 in different concentrations. Cell viability was evaluated by MTT assay for 24 hour and 48 hours. The LD50 value was calculated for the level of cell death and its effectiveness. The dose-dependent manner plays an important role in the treatment of lung cancer cell lines. The present study suggests that Mikania glomerata may be used as an alternative anticancer agent and further research is needed to improve the effectiveness.

scholarly journals Differences in the Relative Abundance of ProBDNF and Mature BDNF in A549 and H1299 Human Lung Cancer Cell Media

2021 ◽  
Vol 22 (13) ◽  
pp. 7059
Author(s):  
Sadaf Dorandish ◽  
Sarah Atali ◽  
Ravel Ray ◽  
Hind Al Khashali ◽  
Kai-Ling Coleman ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Relative Abundance ◽  
Neurotrophic Factor ◽  
A549 Cells ◽  
Brain Derived Neurotrophic Factor ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
H1299 Cell ◽  
The Media

Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, has been linked to several human malignancies and shown to promote tumorigenesis. The purpose of this study was to explore the relative abundance of pro-brain-derived neurotrophic factor (proBDNF) and mature BDNF (mBDNF) in A549 (p53 wild-type) and H1299 (p53-null) lung cancer cell media. Higher levels of proBDNF were detected in the media of A549 cells than in H1299 cell media. Using inhibitors, we found that the levels of proBDNF and mBDNF in the media are likely regulated by PI3K, AKT, and NFκB. However, the largest change in these levels resulted from MMP2/9 inhibition. Blocking p53 function in A549 cells resulted in increased mBDNF and decreased proBDNF, suggesting a role for p53 in regulating these levels. The ratio of proBDNF/mBDNF was not affected by MMP2 knockdown but increased in the media of both cell lines upon knockdown of MMP9. Downregulation of either MMP2 or MMP9 by siRNA showed that MMP9 siRNA treatment of either A549 or H1299 cells resulted in decreased cell viability and increased apoptosis, an effect diminished upon the same treatment with proBDNF immunodepleted media, suggesting that MMP9 regulates the cytotoxic effects induced by proBDNF in lung cancer cells.

scholarly journals Construction of Radiation Surviving/Resistant Lung Cancer Cell Lines with Equidifferent Gradient Dose Irradiation

Dose-Response ◽  
2020 ◽  
Vol 18 (4) ◽  
pp. 155932582098242
Author(s):  
Lijuan Wang ◽  
Shangbiao Li ◽  
Xiaoxia Zhu
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Radiation Resistance ◽  
Cancer Cell Lines ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Dose Irradiation ◽  
Dose Dependent

Radiotherapy plays an increasingly crucial role in the treatment of non-small cell lung cancer (NSCLC). Local tumor recurrence and tumor progression caused by intratumoral heterogeneity induced radiotherapy resistance remain the primary causes of radiotherapy failure. However, the lack of a suitable cell line model has hampered the exploration of the dynamic mechanisms of radiation resistance. We established 3 groups of equidifferent gradient dose irradiation surviving/resistant human lung cancer cell lines based on A549, H520, and H460 cells with clinical conventional fractionated radiotherapy (CFRT) (2 Gy × 20 F, 2 Gy × 30 F, and 2 Gy × 40 F). The radiosensitivity of the cells was detected by clone formation assay, EDU cell proliferation assay, neutral comet assay, and γ-H2AX immunofluorescence staining. The radiosensitivity and proliferation viability were increased in a received dose-dependent manner. Compared with parental cells, DNA double-strand breaks (DSBs) in cell lines that received higher-dose irradiation were significantly reduced. We successfully constructed equidifferent gradient dose irradiation surviving/resistant NSCLC cell lines whose radiation surviving and resistant abilities were increased in a received dose-dependent manner. This preclinical cell model could be used to dynamically observe and detect the radiation surviving/resistant biomarkers during radiotherapy stress, elucidate the mechanism of radiation resistance.

scholarly journals ZAK inhibits human lung cancer cell growth via ERK and JNK activation in an AP-1-dependent manner

2010 ◽  
Vol 101 (6) ◽  
pp. 1374-1381 ◽  
Author(s):  
Jaw-Ji Yang ◽  
Yi-Ju Lee ◽  
Hsin-Hung Hung ◽  
Wei-Pu Tseng ◽  
Chuan-Chou Tu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cell ◽  
Jnk Activation

3,4,5-Trihydroxybenzoic Acid Triggered Oxidative Stress in 95-D Lung Cancer Cell Line

2014 ◽  
Vol 926-930 ◽  
pp. 1061-1064
Author(s):  
Yan Li Xi ◽  
Xiang Qun Wu ◽  
Jie Yu ◽  
Wei Guo Xu ◽  
Tong Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell

It is a good therapeutic method that add exogenous ROS to trigger oxidative stress causing death of cancer cells. In the present study, we investigated the inhibitory effects of 3,4,5-trihydroxybenzoic acid (TBA), a polyhydroxyphenolic compound, on high metastatic human lung cancer cell line (95-D) based on inducing reactive oxygen species (ROS). The experiments in vitro showed that 95-D cell viability was inhibited by various amounts of TBA and death was induced in a dose-dependent manner. The possible mechanism was that TBA can induce cell death by decreasing mitochondrial membrane potential (MMP; ΔΨm) and increasing hydrogen peroxide (H2O2) level. These results imply that TBA efficiently induces death in 95-D lung cancer cells and that TBA exerts cytotoxicity on cancer cells by its pro-oxidative activity.

scholarly journals Inhibition of A549 Lung Cancer Cell Migration and Invasion by Ent-Caprolactin C via the Suppression of Transforming Growth Factor-β-Induced Epithelial—Mesenchymal Transition

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 465
Author(s):  
So Young Kim ◽  
Myoung-Sook Shin ◽  
Geum Jin Kim ◽  
Hyukbean Kwon ◽  
Myong Jin Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Cancer Cell ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Transforming Growth Factor Β ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Mesenchymal Transition

The epithelial–mesenchymal transition (EMT) of cancer cells is a crucial process in cancer cell metastasis. An Aquimarina sp. MC085 extract was found to inhibit A549 human lung cancer cell invasion, and caprolactin C (1), a new natural product, α-amino-ε-caprolactam linked to 3-methyl butanoic acid, was purified through bioactivity-guided isolation of the extract. Furthermore, its enantiomeric compound, ent-caprolactin C (2), was synthesized. Both 1 and 2 inhibited the invasion and γ-irradiation-induced migration of A549 cells. In transforming growth factor-β (TGF-β)-treated A549 cells, 2 inhibited the phosphorylation of Smad2/3 and suppressed the EMT cell marker proteins (N-cadherin, β-catenin, and vimentin), as well as the related messenger ribonucleic acid expression (N-cadherin, matrix metalloproteinase-9, Snail, and vimentin), while compound 1 did not suppress Smad2/3 phosphorylation and the expression of EMT cell markers. Therefore, compound 2 could be a potential candidate for antimetastatic agent development, because it suppresses TGF-β-induced EMT.

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