scholarly journals Highly efficient radiosensitization of human glioblastoma and lung cancer cells by a G-quadruplex DNA binding compound

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Patrick Merle ◽  
Marine Gueugneau ◽  
Marie-Paule Teulade-Fichou ◽  
Mélanie Müller-Barthélémy ◽  
Simon Amiard ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Human Glioblastoma ◽  
Quadruplex Dna ◽  
Highly Efficient ◽  
G Quadruplex

scholarly journals Mitogenic Effect of Orphan Receptor TR3 and Its Regulation by MEKK1 in Lung Cancer Cells

2003 ◽  
Vol 23 (23) ◽  
pp. 8651-8667 ◽  
Author(s):  
Siva Kumar Kolluri ◽  
Nathalie Bruey-Sedano ◽  
Xihua Cao ◽  
Bingzhen Lin ◽  
Feng Lin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Cellular Localization ◽  
Ectopic Expression ◽  
Orphan Receptor ◽  
Lung Cancer Cells ◽  
Brdu Incorporation ◽  
Mitogenic Effect ◽  
Retinoid Receptor

ABSTRACT TR3, also known as NGFI-B or nur77, is an immediate-early response gene and an orphan member of the steroid/thyroid/retinoid receptor superfamily. We previously reported that TR3 expression was induced by apoptotic stimuli and was required for their apoptotic effect in lung cancer cells. Here, we present evidence that TR3 was also induced by epidermal growth factor (EGF) and serum and was required for their mitogenic effect in lung cancer cells. Ectopic expression of TR3 in both H460 and Calu-6 lung cancer cell lines promoted their cell cycle progression and BrdU incorporation, while inhibition of TR3 expression by the small interfering RNA approach suppressed the mitogenic effect of EGF and serum. Analysis of TR3 mutants showed that both TR3 DNA binding and transactivation were required for its mitogenic effect. In contrast, they were dispensable for its apoptotic activity. Furthermore, confocal microscopy analysis demonstrated that TR3 functioned in the nucleus to induce cell proliferation, whereas it acted on mitochondria to induce apoptosis. In examining the signaling that regulates the mitogenic function of TR3, we observed that coexpression of constitutive-active MEKK1 inhibited TR3 transcriptional activity and TR3-induced proliferation. The inhibitory effect of MEKK1 was mediated through activation of Jun N-terminal kinase, which efficiently phosphorylated TR3, resulting in loss of its DNA binding. Together, our results demonstrate that TR3 is capable of inducing both proliferation and apoptosis in the same cells depending on the stimuli and its cellular localization.

The biological activity of G-quadruplex DNA binding papaverine-derived ligand in breast cancer cells

2008 ◽  
Vol 27 (4) ◽  
pp. 289-296 ◽  
Author(s):  
Blazej Rubis ◽  
Mariusz Kaczmarek ◽  
Natalia Szymanowska ◽  
Elzbieta Galezowska ◽  
Andrzej Czyrski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Biological Activity ◽  
Dna Binding ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Quadruplex Dna ◽  
G Quadruplex

Syntheses, structural characterization and biological activities of spiro-ansa-spiro-cyclotriphosphazenes

2015 ◽  
Vol 39 (11) ◽  
pp. 8825-8839 ◽  
Author(s):  
Nisan Sevin Başterzi ◽  
Selen Bilge Koçak ◽  
Aytuğ Okumuş ◽  
Zeynel Kılıç ◽  
Tuncer Hökelek ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Structural Characterization ◽  
Biological Activities ◽  
Antimicrobial Activities ◽  
Lung Cancer Cells

spiro-ansa-spiro-Phosphazenes were investigated for their DNA binding, antimicrobial activities and cytotoxic, apoptotic, and necrotic effects on fibroblast and lung cancer cells.

Synthesis, DNA binding and antiproliferative activity of ternary copper complexes of moxifloxacin and gatifloxacin against lung cancer cells

2012 ◽  
Vol 23 ◽  
pp. 78-84 ◽  
Author(s):  
Rinky Singh ◽  
Ravirajsinh N. Jadeja ◽  
Menaka C. Thounaojam ◽  
Tushar Patel ◽  
Ranjitsinh V. Devkar ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Antiproliferative Activity ◽  
Copper Complexes ◽  
Lung Cancer Cells

Inhibitory effects of Actinidia Chinensis planch root extracts (acRoots) on human lung cancer cells through retinoic acid receptor beta

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Retinoic Acid Receptor ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Inhibitory Effects ◽  
The Core ◽  
Human Lung Cancer Cells ◽  
Receptor Beta

Actinidia Chinensis Planch roots (acRoots) are used to treat many cancers, although the anti-tumor mechanism by which acRoots inhibit cancer cell growth remains unclear. The present study aims at investigating inhibitory effects of acRoots on human lung cancer cells and potential mechanisms. Our data demonstrate that the inhibitory effects of acRoots on lung cancer cells depend on genetic backgrounds and phenotypes of cells. We furthermore found the expression of metabolism-associated gene profiles varied between acRoots-hypersensitive (H460) or hyposensitive lung cancer cells (H1299) after screening lung cancer cells with different genetic backgrounds. We selected retinoic acid receptor beta (RARB) as the core target within metabolism-associated core gene networks and evaluated RARB changes and roles in cells treated with acRoots at different concentrations and timeframes. Hypersensitive cancer cells with the deletion of RARB expression did not response to the treatment with acRoots, while RARB deletion did not change effects of acRoots on hyposensitive cells. Thus, it seems that RARB as the core target within metabolism-associated networks plays important roles in the regulation of lung cancer cell sensitivity to acRoots.

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