A novel biocompatible formate bridged 1D-Cu(ii) coordination polymer induces apoptosis selectively in human lung adenocarcinoma (A549) cells

2021 ◽  
Vol 50 (6) ◽  
pp. 2253-2267
Author(s):  
Mohammad Usman ◽  
Rais Ahmad Khan ◽  
Mohammad Rashid Khan ◽  
Mohammad Abul Farah ◽  
Ibtisam I. BinSharfan ◽  
...  
Keyword(s):  
Coordination Polymer ◽  
Lung Adenocarcinoma ◽  
Anticancer Drugs ◽  
Human Lung ◽  
A549 Cells ◽  
Next Generation ◽  
Human Lung Adenocarcinoma ◽  
Copper Compounds ◽  
Lung Adenocarcinoma A549

Copper compounds are promising candidates for next-generation metal anticancer drugs.

scholarly journals Increase in Toxicity of Anticancer Drugs by PMTPV, a Claudin-1-Binding Peptide, Mediated via Down-Regulation of Claudin-1 in Human Lung Adenocarcinoma A549 Cells

2020 ◽  
Vol 21 (16) ◽  
pp. 5909
Author(s):  
Haruka Nasako ◽  
Yui Takashina ◽  
Hiroaki Eguchi ◽  
Ayaka Ito ◽  
Yoshinobu Ishikawa ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Anticancer Drugs ◽  
Human Lung ◽  
Lucifer Yellow ◽  
Mrna Level ◽  
Three Dimensional ◽  
A549 Cells ◽  
Human Lung Adenocarcinoma ◽  
Lung Adenocarcinoma A549 ◽  
Resistant Cells

Claudin-1 (CLDN1), a tight junctional protein, is highly expressed in lung cancer cells and may contribute to chemoresistance. A drug which decreases CLDN1 expression could be a chemosensitizer for enhancing the efficacy of anticancer drugs, but there is no such drug known. We found that PMTPV, a short peptide, which mimics the structure of second extracellular loop (ECL2) of CLDN1, can reduce the protein level of CLDN1 without affecting the mRNA level in A549 cells derived from human lung adenocarcinoma. The PMTPV-induced decrease in CLDN1 expression was inhibited by monodansylcadaverine, a clathrin-mediated endocytosis inhibitor, and chloroquine, a lysosome inhibitor. Quartz crystal microbalance assay showed that PMTPV can directly bind to the ECL2 of CLDN1. In transwell assay, PMTPV increased fluxes of Lucifer yellow (LY), a paracellular flux marker, and doxorubicin (DXR), an anthracycline anticancer drug, without affecting transepithelial electrical resistance. In three-dimensional spheroid culture, the size and cell viability were unchanged by short peptides, but the fluorescence intensity of hypoxia probe LOX-1 was decreased by PMTPV. PMTPV elevated the accumulation and cytotoxicity of DXR in the spheroids. Similar results were observed by knockdown of CLDN1. Furthermore, the sensitivities to cisplatin (CDDP), docetaxel, and gefitinib were enhanced by PMTPV. The level of CLDN1 expression in CDDP-resistant cells was higher than that in parental A549 cells, which was reduced by PMTPV. PMTPV restored the toxicity to DXR in the CDDP-resistant cells. Our data suggest that PMTPV may become a novel chemosensitizer for lung adenocarcinoma.

scholarly journals Upregulation of Chemoresistance by Mg2+ Deficiency through Elevation of ATP Binding Cassette Subfamily B Member 1 Expression in Human Lung Adenocarcinoma A549 Cells

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1179
Author(s):  
Saki Onuma ◽  
Aya Manabe ◽  
Yuta Yoshino ◽  
Toshiyuki Matsunaga ◽  
Tomohiro Asai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Anticancer Drugs ◽  
Human Lung ◽  
A549 Cells ◽  
Atp Binding ◽  
G1 Arrest ◽  
Human Lung Adenocarcinoma ◽  
Lung Adenocarcinoma A549 ◽  
Atp Binding Cassette

Several anticancer drugs including cisplatin (CDDP) induce hypomagnesemia. However, it remains fully uncertain whether Mg2+ deficiency affects chemosensitivity of cancer cells. Here, we investigated the effect of low Mg2+ concentration (LM) on proliferation and chemosensitivity using human lung adenocarcinoma A549 cells. Cell proliferation was reduced by continuous culture with LM accompanied with the elevation of G1 phase proportion. The amounts of reactive oxygen species (ROS) and stress makers such as phosphorylated-ataxia telangiectasia mutated and phosphorylated-p53 were increased by LM. Cell injury was dose-dependently increased by anticancer drugs such as CDDP and doxorubicin (DXR), which were suppressed by LM. Similar results were obtained by roscovitine, a cell cycle inhibitor. These results suggest that LM induces chemoresistance mediated by ROS production and G1 arrest. The mRNA and protein levels of ATP binding cassette subfamily B member 1 (ABCB1) were increased by LM and roscovitine. The LM-induced elevation of ABCB1 and nuclear p38 expression was suppressed by SB203580, a p38 MAPK inhibitor. PSC833, an ABCB1 inhibitor, and SB203580 rescued the sensitivity to anticancer drugs. In addition, cancer stemness properties were suppressed by SB203580. We suggest that Mg2+ deficiency reduces the chemotherapy sensitivity of A549 cells, although it suppresses cell proliferation.

scholarly journals Biological Evaluation of Alkyl Triphenylphosphonium Ostruthin Derivatives as Potential Anti-Inflammatory Agents Targeting the Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

BioChem ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 107-121
Author(s):  
Nghia Trong Vo ◽  
Eiichi Kusagawa ◽  
Kaori Nakano ◽  
Chihiro Moriwaki ◽  
Yasunobu Miyake ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Human Lung ◽  
A549 Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Human Lung Adenocarcinoma ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Lung Adenocarcinoma A549

Ostruthin (6-geranyl-7-hydroxycoumarin) is one of the constituents isolated from Paramignya trimera and has been classified as a simple coumarin. We recently reported the synthesis of alkyl triphenylphosphonium (TPP) derivatives from ostruthin and evaluated their anticancer activities. In the present study, we demonstrated that alkyl TPP ostruthin derivatives inhibited the up-regulation of cell-surface intercellular adhesion molecule-1 (ICAM-1) in human lung adenocarcinoma A549 cells stimulated with tumor necrosis factor-α (TNF-α) without affecting cell viability, while ostruthin itself exerted cytotoxicity against A549 cells. The heptyl TPP ostruthin derivative (termed OS8) attenuated the up-regulation of ICAM-1 mRNA expression at concentrations higher than 40 µM in TNF-α-stimulated A549 cells. OS8 inhibited TNF-α-induced nuclear factor κB (NF-κB)-responsive luciferase reporter activity at concentrations higher than 40 µM, but did not affect the translocation of the NF-κB subunit RelA in response to the TNF-α stimulation at concentrations up to 100 µM. A chromatin immunoprecipitation assay showed that OS8 at 100 µM prevented the binding of RelA to the ICAM-1 promoter. We also showed that OS8 at 100 µM inhibited the TNF-α-induced phosphorylation of RelA at Ser 536. Moreover, the TNF-α-induced phosphorylation of an inhibitor of NF-κB α and extracellular signal-regulated kinase was reduced by OS8. These results indicate that OS8 has potential as an anti-inflammatory agent that targets the NF-κB signaling pathway.

scholarly journals Gene expression profiling of cancer stem cell in human lung adenocarcinoma A549 cells

2007 ◽  
Vol 6 (1) ◽  
pp. 75 ◽  
Author(s):  
Dong-Cheol Seo ◽  
Ji-Min Sung ◽  
Hee-Jung Cho ◽  
Hee Yi ◽  
Kun-Ho Seo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Lung Adenocarcinoma ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Adenocarcinoma ◽  
Lung Adenocarcinoma A549
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