scholarly journals Human Lung Cancer Cell Line A-549 ATCC Is Differentially Affected by Supranutritional Organic and Inorganic Selenium

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Lérida Liss Flores Villavicencio ◽  
Gustavo Cruz-Jiménez ◽  
Gloria Barbosa-Sabanero ◽  
Carlos Kornhauser-Araujo ◽  
M. Eugenia Mendoza-Garrido ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Nuclear Fragmentation ◽  
Inorganic Selenium

The effects of organic and inorganic forms of selenium (Se) on human cells have been extensively studied for nutritional concentrations; however, to date, little is known about the potential toxicity at supranutritional levels. In the present study we determined the effects of sodium selenite (SSe) and selenomethionine (SeMet) on cell growth and intracellular structures in lung cancer cells exposed at Se concentrations between 0 and 3 mM. Our results showed that SSe affected cell growth more rapidly than SeMet (24 h and 48 h, resp.). After 24 h of cells exposure to 0.5, 1.5, and 3 mM SSe, cell growth was reduced by 10, 50, and 60%, as compared to controls. After 48 h, nuclear fragmentation was evident in cells exposed to SSe, suggesting an induction to cell death. In contrast, SeMet did not affect cell proliferation, and the cells were phenotypically similar to controls. Microtubules and microfilaments structures were also affected by both Se compounds, again SSe being more toxic than SeMet. To our knowledge, this is the first report on the differential effects of organic and inorganic Se in supranutritional levels in lung cancer cells.

Purification of a cell growth factor from a human lung cancer cell line: Its relationship with ferritin

1994 ◽  
Vol 161 (1) ◽  
pp. 106-110 ◽  
Author(s):  
Nobuaki Kikyo ◽  
Koichi Hagiwara ◽  
Michio Fujisawa ◽  
Nobuko Kikyo ◽  
Yoshio Yazaki ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Cell Line ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
A Cell

The Rhizome of Trillium tschonoskii Maxim. Extract Induces Apoptosis in Human Lung Cancer Cells

2011 ◽  
Vol 66 (9-10) ◽  
pp. 477-484 ◽  
Author(s):  
Wenfeng Huang ◽  
Kun Zou ◽  
Bin Xiong
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Butanol Extract ◽  
Human Lung Cancer Cells ◽  
Trillium Tschonoskii

Trillium tschonoskii Maxim. has been used to treat several diseases including cancers in folk medicine. However, the mechanisms responsible for T. tschonoskii extract-induced apoptosis are not clear. This study was mainly undertaken to identify the major biochemical changes in a lung cancer cell line upon treatment with an T. tschonoskii extract (TTME), and to investigate the functional relationship between these changes. The n-butanol extract was used to evaluate the mechanism of induction of apoptosis in A549 human lung cancer cells and its effects on mitochondrial function and production of reactive oxygen species (ROS). The n-butanol extract of T. tschonoskii has cytotoxic, antiproliferative, and morphological effects on the lung cancer cell line. T. tschonoskii mainly leads to apoptosis of cancer cells with a concomitant increase in the release of cytochrome c and a loss of mitochondrial membrane potential in a dose-dependent manner. A rapid increase in the level of intracellular ROS and an accumulation of cells in the G2/M and S phase of the cell cycle were also observed in treated cells. These observations suggest that the n-butanol extract of T. tschonoskii has promising anticancer activities, which could be useful in cancer treatment.

scholarly journals Radix Glehniae extract inhibits migration and invasion of lung cancer cells

2018 ◽  
Vol 6 (2) ◽  
pp. 48-53 ◽  
Author(s):  
Wang Zhen-fei ◽  
Liu Li ◽  
Liang Lin ◽  
Hao Qin
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Enzyme Linked Immunosorbent Assay ◽  
Lung Cancer Cell

Abstract Objective The aim of this study was to investigate the effect of Radix Glehniae on the migration and invasion abilities of lung cancer cells. Methods Normal bronchial cell line 16HBE and lung cancer cell line SK-MES-1 were treated with Radix Glehniae extract. Proliferation, migration, and invasion abilities were determined by Cell Counting Kit (CCK)-8, Transwell, and Matrigel assays, respectively. The expression and secretion levels of tissue inhibitor of metalloproteinases 2 were detected by quantitative PCR and enzyme-linked immunosorbent assay, respectively. Results Radix Glehniae extract inhibited the migration and invasion abilities of SK-MES-1 cells and enhanced TIMP2 expression and secretion by SK-MES-1 cells, without causing toxicity to 16HBE cells. Conclusion Radix Glehniae is useful in lung cancer treatment.

scholarly journals Beclin1-induced Autophagy Abrogates Radioresistance of Lung Cancer Cells by Suppressing Osteopontin

2012 ◽  
Vol 53 (3) ◽  
pp. 422-432 ◽  
Author(s):  
Seung-Hee Chang ◽  
Arash Minai-Tehrani ◽  
Ji-Young Shin ◽  
Sungjin Park ◽  
Ji-Eun Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Human Lung Cancer Cells

Abstract Osteopontin (OPN) serves as an indicator of resistance to radiotherapy. However, the role of OPN in the development of acquired radioresistance in human lung cancer cells has not yet been fully elucidated. Therefore, the potential importance of OPN as a marker of lung cancer with a potential significant role in the development of radioresistance against repeated radiotherapy has prompted us to define the pathways by which OPN regulates lung cancer cell growth. In addition, autophagy has been reported to play a key role in the radiosensitization of cancer cells. Here, we report that increased OPN expression through induction of nuclear p53 following irradiation was inhibited by exogenous beclin-1 (BECN1). Our results clearly show that BECN1 gene expression led to induction of autophagy and inhibition of cancer cell growth and angiogenesis. Our results suggest that the induction of autophagy abrogated the radioresistance of the cancer cells. Interestingly, we showed that knockdown of OPN by lentivirus-mediated shRNA induced the autophagy of human lung cancer cell. Taken together, these results suggest that OPN and BECN1 can be molecular targets for overcoming radioresistance by controlling autophagy.

scholarly journals Knockdown of autophagy-related gene BECLIN1 promotes cell growth and inhibits apoptosis in the A549 human lung cancer cell line

2013 ◽  
Vol 7 (5) ◽  
pp. 1501-1505 ◽  
Author(s):  
WENYU WANG ◽  
HONGKUN FAN ◽  
YUN ZHOU ◽  
PING DUAN ◽  
GUOQIANG ZHAO ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cell Line ◽  
Cancer Cell ◽  
Human Lung ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Human Lung Cancer ◽  
Related Gene ◽  
Lung Cancer Cell

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 c-Jun N-Terminal Kinase Contributes to Aberrant Retinoid Signaling in Lung Cancer Cells by Phosphorylating and Inducing Proteasomal Degradation of Retinoic Acid Receptor α

2005 ◽  
Vol 25 (3) ◽  
pp. 1054-1069 ◽  
Author(s):  
Harish Srinivas ◽  
Denise M. Juroske ◽  
Shailaja Kalyankrishna ◽  
Dianna D. Cody ◽  
Roger E. Price ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Retinoid Signaling ◽  
Phosphopeptide Mapping

ABSTRACT Retinoic acid (RA) is the ligand for nuclear RA receptors (RARs and RXRs) and is crucial for normal epithelial cell growth and differentiation. During malignant transformation, human bronchial epithelial cells acquire a block in retinoid signaling caused in part by a transcriptional defect in RARs. Here, we show that activation of c-Jun N-terminal kinase (JNK) contributes to RAR dysfunction by phosphorylating RARα and inducing degradation through the ubiquitin-proteasomal pathway. Analysis of RARα mutants and phosphopeptide mapping revealed that RARα residues Thr181, Ser445, and Ser461 are phosphorylated by JNK. Mutation of these residues to alanines prevented efficient ubiquitination of RARα and increased the stability of the protein. We investigated the importance of RARα phosphorylation by JNK as a mediator of retinoid resistance in lung cancer. Mice that develop lung cancer from activation of a latent K-ras oncogene had high intratumoral JNK activity and low RARα levels and were resistant to treatment with an RAR ligand. JNK inhibition in a human lung cancer cell line enhanced RARα levels, ligand-induced activity of RXR-RAR dimers, and growth inhibition by RA. These findings point to JNK as a key mediator of aberrant retinoid signaling in lung cancer cells.

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