Nanogold POxylation: towards always-on fluorescent lung cancer targeting

RSC Advances ◽  
2016 ◽  
Vol 6 (40) ◽  
pp. 33631-33635 ◽  
Author(s):  
A. Sofia Silva ◽  
Marta C. Silva ◽  
Sónia P. Miguel ◽  
Vasco D. B. Bonifácio ◽  
Ilídio J. Correia ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Gold Nanoparticles ◽  
Cell Line ◽  
A549 Cell ◽  
Cancer Targeting ◽  
A549 Cell Line ◽  
Line P

Gold nanoparticles (GNPs) were POxylated with fluorescent oligomers, synthesized in supercritical CO2, and conjugated with a laminin fragment. Particle design strongly impacts on probes uptake by the A549 cell line.

Dynamic interconversion between CD90+ and CD90− cancer cell populations in lung cancer A549 cell line

2018 ◽  
Vol 14 (5) ◽  
pp. 1822
Author(s):  
Wai-Kin Yu ◽  
Yuen-San Chan ◽  
Weimao Wang ◽  
Chi-chun Fong ◽  
Tak-Chun Yip ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
Cancer Cell ◽  
A549 Cell ◽  
Cell Populations ◽  
A549 Cell Line ◽  
Lung Cancer A549 Cell

scholarly journals Valproic acid inhibit non-small-cell lung cancer (A549 cell line) metastasis via inhibition of CD44v6 and Nm23H1

2019 ◽  
Author(s):  
Sorush Niknamian
Keyword(s):  
Lung Cancer ◽  
Valproic Acid ◽  
Cell Line ◽  
Histone Deacetylase ◽  
A549 Cell ◽  
Histone Deacetylase Inhibitors ◽  
Caspase 3 ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
A549 Cell Line

Currently, epigenetic changes are considered to be one of the most important factors in the incidence of cancer and its metastasis to various tissues. It has been shown that CD44v6 and Nm23-H1 genes play a crucial role in the metastasis of various cancers. However, no study has been done on the effect of epigenetic factors on the expression of CD44v6 and Nm23-H1 genes in the lung cancer cell line, A549.Therefore, the present study investigated the role of a histone deacetylase inhibitor, valproic acid, on the expression of CD44v6 and Nm23-H1 genes and proteins in the A549 cell line. In this study, the A549 cell line was treated with valproic acid at concentrations of 2.2 mM, 4.5 mM, and 9 mM. We then investigated the expression of CD44v6 and Nm23-H1 genes and proteins, as well as the expression of MMP-2 and MMP-9 genes and caspase-3 activity. The results showed that valproic acid significantly decreased the expression of CD44v6 gene and protein and MMP-2 and MMP-9 genes, but increased the expression of Nm23H1 gene and protein and the activity of caspase-3 (p˂ 0.05). Our results showed that histone deacetylases affected the expression of CD44v6, Nm23-H1, MMP-2, and MMP-9, which are involved in metastasis. Therefore, the use of histone deacetylase inhibitors can be effective in the suppression of metastases and the treatment of lung cancer.

scholarly journals Synthesis, Characterization and Anticancer Activity of Transition Metal Substituted Polyoxometalate-β-Cyclodextrin Composites

2019 ◽  
Vol 32 (2) ◽  
pp. 297-302 ◽  
Author(s):  
Bharath Samannan ◽  
Jothi Selvam ◽  
Jeyabalan Thavasikani
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
A549 Cell ◽  
A549 Cell Line ◽  
X Ray Diffraction ◽  
Minimum Concentration ◽  
X Ray ◽  
Ic50 Value ◽  
Ft Ir ◽  
Lung Cancer A549 Cell

A novel hybrid composite, namely {[VIV+PMo11O40]⊂[β-CD]} which shows the high percent of apoptosis of MTT assay of A549 cell line (lung cancer) in different concentrations. The composite has been characterized using techniques such as FT-IR, EPR, SEM, EDS and X-ray diffraction. The anticancer (lung cancer A549 cell line) was investigated using direct microscopic observations for drug treated cell line and IC50 value of 1.93. The apoptosis of 45.37 % cell death in cell line of minimum concentration (3.12 μg/mL) shows the good viability of β-CD-POM against lung cancer A549 cell line.

scholarly journals Pinus massoniana bark extract inhibits migration of the lung cancer A549 cell line

2016 ◽  
Vol 13 (2) ◽  
pp. 1019-1023 ◽  
Author(s):  
Ping Mao ◽  
Ershao Zhang ◽  
Yang Chen ◽  
Likun Liu ◽  
Daqing Rong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
A549 Cell ◽  
Pinus Massoniana ◽  
Bark Extract ◽  
A549 Cell Line ◽  
Lung Cancer A549 Cell

scholarly journals Promising Anticancer Effect of Aurisin A Against the Human Lung Cancer A549 Cell Line

2020 ◽  
Vol 21 (1) ◽  
pp. 49-54
Author(s):  
Parichart Boueroy ◽  
Thidarut Boonmars ◽  
Somdej Kanokmedhakul ◽  
Sorujsiri Chareonsudjai ◽  
Ratsami Lekphrom ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
A549 Cell ◽  
Human Lung ◽  
Human Lung Cancer ◽  
A549 Cell Line ◽  
Anticancer Effect ◽  
Lung Cancer A549 Cell

scholarly journals Evaluation of the Cytotoxic Effect of Ellagic Acid Nanocomposite in Lung Cancer A549 Cell Line and RAW 264.9 Cells

2017 ◽  
Vol 11 (6) ◽  
pp. 578-583
Author(s):  
Samer Hasan Hussein-Al-Ali ◽  
Mothanna Al-Qubaisi ◽  
Abdullah Rasedee ◽  
Mohd Zobir Hussein
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
A549 Cell ◽  
Ellagic Acid ◽  
Cytotoxic Effect ◽  
A549 Cell Line ◽  
Lung Cancer A549 Cell

scholarly journals Loss-of-function mutations in KEAP1 drive lung cancer progression via KEAP1/NRF2 pathway activation

2020 ◽  
Author(s):  
Meiling Gong ◽  
Yan Li ◽  
Xiao-Ping Ye ◽  
Linlin Zhang ◽  
Zhifang Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Line ◽  
Cell Lines ◽  
A549 Cell ◽  
Somatic Mutations ◽  
Lung Squamous Cell Carcinoma ◽  
In Vivo Studies ◽  
Related Factor ◽  
A549 Cell Line ◽  
Loss Of Function

Abstract Background and Purpose: Targeted therapy and immunotherapy have led to dramatic change in the treatment of lung cancer, however, the overall 5-year survival rate of lung cancer patients is still suboptimal. It is important to exploit new potential of molecularly targeted therapies. High-frequency somatic mutations in KEAP1/NRF2 (27.9%) have been identified in lung squamous cell carcinoma. In this research, we explored the role of KEAP1 somatic mutations in the development of LSCC and whether a nuclear factor erythroid 2-related factor 2(NRF2) inhibitor be potential to targetlung cancer carrying KEAP1/NRF2 mutations. Methods: Lung cancer cell lines A549 and H460 with loss-of-function mutations in KEAP1 stably transfected with wild-type (WT) KEAP1 or somatic mutations in KEAP1 were used to investigate the functions of somatic mutations in KEAP1 . Flow cytometry, plate clone formation experiments, and scratch tests were used to examine reactive oxygen species, proliferation, and migration of these cell lines. Results: The expression of NRF2 and its target genes increased , and tumor cell proliferation, migration, and tumor growth were accelerated in A549 and H460 cells stably transfected with KEAP1 mutants compared to control cells with a loss-of-function KEAP1 mutation and stably transfected with WT KEAP1 in both in vitro and in vivo studies. The proliferation of A549 cell line trasfected with the R320Q KEAP1 mutant was Inhibited more apparent than that of the A549 cell line trasfected with WT KEAP1 after treatment with NRF2 inhibitor ML385. Conclusion : Somatic mutations of KEAP1 identified from patients with LSCC likely promote tumorigenesis mediated by activation of the KEAP1/NRF2 antioxidant stress response pathway. NRF2 inhibition with ML385 could inhibit the proliferation of tumor cells with KEAP1 mutation.

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