scholarly journals A Novel Use of Gentamicin in the ROS-Mediated Sensitization of NCI-H460 Lung Cancer Cells to Various Anticancer Agents

2013 ◽  
Vol 8 (12) ◽  
pp. 2771-2777 ◽  
Author(s):  
Michael F. Cuccarese ◽  
Amit Singh ◽  
Mansoor Amiji ◽  
George A. O’Doherty
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Lung Cancer Cells

scholarly journals Photochemical generation of the 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) radical from caged nitroxides by near-infrared two-photon irradiation and its cytocidal effect on lung cancer cells

2019 ◽  
Vol 15 ◽  
pp. 863-873 ◽  
Author(s):  
Ayato Yamada ◽  
Manabu Abe ◽  
Yoshinobu Nishimura ◽  
Shoji Ishizaka ◽  
Masashi Namba ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Near Infrared ◽  
Lung Cancer Cells ◽  
Quantum Yields ◽  
Triggered Release ◽  
Two Photon ◽  
Cytocidal Effect ◽  
Tempo Radical

Novel caged nitroxides (nitroxide donors) with near-infrared two-photon (TP) responsive character, 2,2,6,6-tetramethyl-1-(1-(2-(4-nitrophenyl)benzofuran-6-yl)ethoxy)piperidine (2a) and its regioisomer 2b, were designed and synthesized. The one-photon (OP) (365 ± 10 nm) and TP (710–760 nm) triggered release (i.e., uncaging) of the 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO) radical under air atmosphere were discovered. The quantum yields for the release of the TEMPO radical were 2.5% (2a) and 0.8% (2b) in benzene at ≈1% conversion of 2, and 13.1% (2a) and 12.8% (2b) in DMSO at ≈1% conversion of 2. The TP uncaging efficiencies were determined to be 1.1 GM at 740 nm for 2a and 0.22 GM at 730 nm for 2b in benzene. The cytocidal effect of compound 2a on lung cancer cells under photolysis conditions was also assessed to test the efficacy as anticancer agents. In a medium containing 100 μg mL−1 of 2a exposed to light, the number of living cells decreased significantly compared to the unexposed counterparts (65.8% vs 85.5%).

An oral second-generation proteasome inhibitor oprozomib significantly inhibits lung cancer in a p53 independent manner in vitro

2019 ◽  
Vol 51 (10) ◽  
pp. 1034-1040 ◽  
Author(s):  
Hongge Zhu ◽  
Tianhai Wang ◽  
Zhou Xin ◽  
Yiyi Zhan ◽  
Guoming Gu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Proteasome Inhibitor ◽  
Second Generation ◽  
26S Proteasome ◽  
Lung Cancer Cells ◽  
Independent Manner ◽  
P53 Expression

Abstract The destruction of proteins via the ubiquitin–proteasome system is a multi-step, complex process involving polyubiquitination of substrate proteins, followed by proteolytic degradation by the macromolecular 26S proteasome complex. Inhibitors of the proteasome promote the accumulation of proteins that are deleterious to cell survival and are promising anticancer agents. Oprozomib (OPZ), an oral second-generation proteasome inhibitor, has been shown to inhibit the growth of several cancers in preclinical and clinical trials, including multiple myeloma and head and neck cancers, but its effects on lung cancer has not yet been determined. In this study, we evaluated the inhibitory effects of OPZ on lung cancer cell lines in vitro. The results showed that OPZ significantly suppressed cell proliferation and strongly induced apoptosis in both tested lung cancer cells independent of p53 expression. OPZ was able to cause obvious caspase 3 and PARP cleavages and stabilize p53 and its transcriptional targets p21, PUMA, and Noxa. Moreover, OPZ was capable of sensitizing lung cancer cells to the conventional chemotherapeutic drug cisplatin. Our study provides preclinical data and sheds light on the potential applications of proteasome inhibitor OPZ in lung cancer treatment.

Effect of CPT-11 in combination with other anticancer agents in lung cancer cells

1997 ◽  
Vol 8 (3) ◽  
pp. 231-237 ◽  
Author(s):  
Xin-Hai Pei ◽  
Yoichi Nakanishi ◽  
Koichi Takayama ◽  
Feng Bai ◽  
Masayuki Kawasaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Lung Cancer Cells

Selective Cytotoxic Activity and DNA Damage by an Epoxyalkyl Galactopyranoside

2018 ◽  
Author(s):  
Estefanía Burgos-Morón ◽  
Nuria Pastor ◽  
Manuel Luis Orta ◽  
Julio José Jiménez-Alonso ◽  
Margarita Vega-Holm ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Excision Repair ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Lung Cancer Cells ◽  
Normal Cells

Several clinically useful anticancer drugs selectively kill cancer cells by inducing DNA damage; the genomic instability and DNA repair defects of cancer cells make them more vulnerable than normal cells to the cytotoxicity of DNA-damaging agents. Because epoxide-containing compounds can induce DNA damage, we have used the MTT assay to evaluate the selective cytotoxicity of three epoxyalkyl galactopyranosides against A549 lung cancer cells and MRC-5 lung normal cells. Compound (2S,3S)-2,3-Epoxydecyl 4,6-O-(S)-benzylidene-β-D-galactopyranoside (EDBGP) showed the highest selective anticancer activity and was selected for mechanistic studies. After observing that EDBGP induced cellular DNA damage (comet assay), we found that cells deficient in nucleotide excision repair were hypersensitive to the cytotoxicity of this compound; this suggests that EDBGP may induce bulky DNA adducts. EDBGP did not inhibit glycolysis (glucose consumption and lactate production). Pre-treatment of lung cancer cells with several antioxidants did not reduce the cytotoxicity of EDBGP, thereby indicating that reactive oxygen species do not participate in the anticancer activity of this compound. Finally, EDBGP was screened against a panel of cancer cells and normal cells from several tissues, including three genetically modified skin fibroblasts with increasing degree of malignancy. Our results suggest that epoxyalkyl galactopyranosides are promising lead compounds for the development of new anticancer agents.

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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