Pachymic acid inhibits cell growth and modulates arachidonic acid metabolism in nonsmall cell lung cancer A549 cells

2009 ◽  
Vol 49 (3) ◽  
pp. 271-282 ◽  
Author(s):  
Hui Ling ◽  
Xiaobin Jia ◽  
Yaochun Zhang ◽  
Leslie A. Gapter ◽  
Yin-shan Lim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Arachidonic Acid ◽  
Cell Growth ◽  
Cell Lung Cancer ◽  
Acid Metabolism ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Arachidonic Acid Metabolism ◽  
Pachymic Acid

scholarly journals Adenovirus-mediated E2F-1 gene transfer in nonsmall-cell lung cancer induces cell growth arrest and apoptosis

2002 ◽  
Vol 20 (3) ◽  
pp. 703-709 ◽  
Author(s):  
H. Kuhn ◽  
U. Liebers ◽  
C. Gessner ◽  
A. Schumacher ◽  
C. Witt ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Gene Transfer ◽  
Cell Lung Cancer ◽  
Growth Arrest ◽  
Nonsmall Cell Lung Cancer ◽  
Cell Growth Arrest

scholarly journals A dose- and time-dependent effect of oxythiamine on cell growth inhibition in non-small cell lung cancer

2021 ◽  
Author(s):  
Lin Bai ◽  
Hui-li Zhu
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Critical Role ◽  
A549 Cells ◽  
Small Cell ◽  
Time Dependent ◽  
Dependent Manner ◽  
Small Cell Lung

AbstractThe high mortality rate of non-small-cell lung cancer (NSCLC) is mostly due to the high risk of recurrence. A comprehensive understanding of proliferation mechanisms of NSCLC would remarkably contribute to blocking up the invasion and metastasis of tumor cells. In our previous study, the remarkable decreased activity of Thiamine-dependent enzymes (TDEs), involving in intermediary metabolism responsible for energy production of tumor, was found under conditions of thiamine deficiency in vivo. To explore the effect of Oxythiamine (OT), a TDEs antimetabolite, on cell growth, we co-cultured A549 cells with OT in vitro at various doses (0.1, 1, 10 and 100 μM) and time periods (6, 12, 24 and 48 h) and subsequent cell proliferation and apoptosis assays were performed respectively. Our findings demonstrated that A549 cells proliferation was significantly downregulated by OT treatment in a progressively dose as well as time dependent manner. Inhibition of TDEs resulted in antagonism of lung cancer growth by inducing cells to cease the cycle as well as apoptotic cell death. We concluded a critical role of OT, a TDEs antagonistic compound, indicating the potential target of its practical use.

SAHA Treatment Reveals the Link between Histone Lysine Acetylation and Proteome in Nonsmall Cell Lung Cancer A549 Cells

2013 ◽  
Vol 12 (9) ◽  
pp. 4064-4073 ◽  
Author(s):  
Quan Wu ◽  
Weiqing Xu ◽  
Lejie Cao ◽  
Xin Li ◽  
Tieming He ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Lysine Acetylation ◽  
Histone Lysine

scholarly journals Expression of MiR-608 in Nonsmall Cell Lung Cancer and Molecular Mechanism of Apoptosis and Migration of A549 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Chu Huang ◽  
Weiming Yue ◽  
Lin Li ◽  
Shuhai Li ◽  
Cun Gao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Control Group ◽  
Nsclc Tissue ◽  
Protein Levels ◽  
And Migration ◽  
Induced Apoptosis ◽  
Nsclc Patients

Objective. This Work is aimed at exploring the effect of microRNA (MiR)-608 on the function of nonsmall cell lung cancer (NSCLC) A549 cells and related mechanisms. Methods. Blood samples of 106 NSCLC patients (experimental group) as well as 124 normal people (control group) were selected for relevant investigation. Polymerase chain reaction (PCR) as well as DNA sequencing was used to determine the genotyping of the MiR-608 rs4919510 polymorphism. MiR-608 expression in cells was detected by real-time PCR technology. Western blotting was used to detect changes in protein levels. NSCLC tissues as well as adjacent tissues were explored in 33 patients undergoing surgery. Results. MiR-608 rs4919510 does not influence the incidence of NSCLC patients. In addition, MiR-608 expression was downregulated in the tumor tissue of NSCLC patients, while the transcription factor activating enhancer-binding protein 4 (TFAP4) expression was upregulated. MiR-608 promotes DOX- (Doxorubicin-) induced apoptosis by negatively regulating TFAP4 expression in NSCLC tissue. TFAP4 can significantly inhibit the migration of A549 cells. Conclusion. The findings in this investigation can contribute to the effective treatment of NSCLC patients. Also, the investigation can provide some theoretical support for the application of new targets for NSCLC treatment.

Synergistic Effects of 13-cis Retinoic Acid and Arachidonic Acid Cascade Inhibitors on Growth of Head and Neck Squamous Cell Carcinoma in Vitro

1998 ◽  
Vol 118 (2) ◽  
pp. 159-164 ◽  
Author(s):  
Aaron Spingarn ◽  
Peter G. Sacks ◽  
Daniel Kelley ◽  
Andrew J. Dannenberg ◽  
Stimson P. Schantz
Keyword(s):  
Squamous Cell Carcinoma ◽  
Arachidonic Acid ◽  
Retinoic Acid ◽  
Cell Growth ◽  
Growth Inhibition ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Arachidonic Acid Cascade ◽  
Hnscc Cell

Products of arachidonic acid metabolism can influence normal and malignant cell growth. In vivo, inhibitors of arachidonic acid metabolism have been associated with inhibition of tumor growth, including head and neck squamous cell carcinoma (HNSCC). This has not been evaluated extensively in vitro in an HNSCC model. Therefore we investigated the effects of several arachidonic acid cascade inhibitors (AACIs) (indomethacin, curcumin, phenidone, nordihydroguaiaretic acid, 5,8,11,14-eicosatetraynoic acid, and 13- cisretinoic acid) on the growth of two HNSCC cell lines (MDA 886Ln and 1483). We found that AACIs caused dose-dependent growth inhibition of both cell lines. In an effort to inhibit HNSCC cell growth at lower concentrations of these drugs, we evaluated the effects of a variety of AACIs in combination with 13- cis retinoic acid. We observed synergistic growth inhibition when the drugs were used in all combinations, with the exception of indomethacin. These results suggest that AACIs may have some utility in the direct treatment of HNSCC, and a strategy combining 13- cis retinoic acid with other AACIs may prove to be even more effective.

scholarly journals Apoptosis-Inducing Activity of Marine SpongeHaliclonasp. Extracts Collected from Kosrae in Nonsmall Cell Lung Cancer A549 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Woori Bae ◽  
Hyun Kyung Lim ◽  
Kyoung Mee Kim ◽  
Hyosun Cho ◽  
Sun Yi Lee ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Biological Activities ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Marine Sponges ◽  
Caspase 8 ◽  
Anticancer Properties ◽  
Alternative Materials ◽  
Good Resource

Although various anticancer drugs have been developed for the treatment of nonsmall cell lung cancer, chemotherapeutic efficacy is still limited. Natural products such as phytochemicals have been screened as novel alternative materials, but alternative funds such as marine bioresources remain largely untapped. Of these resources, marine sponges have undergone the most scrutiny for their biological activities, including antiinflammatory, antiviral, and anticancer properties. However, the biological mechanisms of the activities of these marine sponges are still unclear. We investigated the anticancer activity of marine sponges collected from Kosrae in Micronesia and examined their mechanisms of action using nonsmall cell lung cancer A549 cells as a model system. Of 20 specimens, theHaliclonasp. (KO1304-328) showed both dose- and time-dependent cytotoxicity. Further, methanol extracts ofHaliclonasp. significantly inhibited cell proliferation and cell viability. A549 cells treated withHaliclonasp. demonstrated induced expression of c-Jun N-terminal kinase (JNK), p53, p21, caspase-8, and caspase-3. The percentage of apoptotic cells significantly increased in A549 cultures treated withHaliclonasp. These results indicate thatHaliclonasp. induces apoptosis via the JNK-p53 pathway and caspase-8, suggesting that this marine sponge is a good resource for the development of drugs for treatment of nonsmall cell lung cancer.

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