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.

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.

scholarly journals Destruxin B Isolated from Entomopathogenic FungusMetarhizium anisopliaeInduces Apoptosis via a Bcl-2 Family-Dependent Mitochondrial Pathway in Human Nonsmall Cell Lung Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Chun-Chi Wu ◽  
Tzu-Hsiu Chen ◽  
Bing-Lan Liu ◽  
Li-Chen Wu ◽  
Yung-Ching Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Molecular Mechanisms ◽  
Apoptotic Cell ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Mitochondrial Pathway ◽  
Lung Cancer Cells ◽  
Gel Chromatography

Destruxin B, isolated from entomopathogenic fungusMetarhizium anisopliae, is one of the cyclodepsipeptides with insecticidal and anticancer activities. In this study, destruxin B was extracted and purified by ion-exchange chromatography, silica gel chromatography, and semipreparative high-performance liquid chromatography. The potential anticancer effects and molecular mechanisms of destruxin B in human nonsmall cell lung cancer cell lines were characterized. Our results showed that destruxin B induced apoptotic cell death in A549 cells. This event was accompanied by the activation of caspase-2, -3, and -9. Moreover, destruxin B increased the expression level of proapoptotic molecule, PUMA, while decreased antiapoptotic molecule Mcl-1. Additionally, the translocation of Bax from cytosol to mitochondrial membrane was observed upon destruxin B treatment. Knockdown of Bax by shRNA effectively attenuated destruxin-B-triggered apoptosis in A549 cells. Interestingly, similar toxic effects and underlying mechanisms including caspase activation, upregulation of PUMA, and downregulation of Mcl-1 were also observed in a p53-null lung cancer H1299 cell line upon destruxin B treatment. Taken together, our findings suggest that destruxin-B-induced apoptosis in human nonsmall cell lung cancer cells is via a Bcl-2 family-dependent mitochondrial pathway.

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 Terpinen-4-ol Induces Apoptosis in Human Nonsmall Cell Lung Cancer In Vitro and In Vivo

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Chieh-Shan Wu ◽  
Yun-Ju Chen ◽  
Jeremy J. W. Chen ◽  
Jeng-Jer Shieh ◽  
Chia-Hsin Huang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Annexin V ◽  
Nonsmall Cell Lung Cancer ◽  
Antitumor Effects ◽  
Apoptotic Pathway

Terpinen-4-ol, a monoterpene component of the essential oils of several aromatic plants, exhibits antitumor effects. In this study, the antitumor effects of terpinen-4-ol and the cellular and molecular mechanisms responsible for it were evaluated and studied, respectively on human nonsmall cell lung cancer (NSCLC) cells. Our results indicated that terpinen-4-ol elicited a dose-dependent cytotoxic effect, as determined by MTT assay. Increased sub-G1 population and annexin-V binding, activation of caspases 9 and 3, cleavage of poly(ADPribose) polymerase (PARP), and a decrease of mitochondrial membrane potential (MMP) indicated involvement of the mitochondrial apoptotic pathway in terpinen-4-ol-treated A549 and CL1-0 cells. Elevation of the Bax/Bcl-2 ratio and a decrease in IAP family proteins XIAP and survivin were also observed following terpinen-4-ol treatment. Notably, terpinen-4-ol was able to increase p53 levels in A549 and CL1-0 cells. Diminution of p53 by RNA interference induced necrosis instead of apoptosis in A549 cells following terpinen-4-ol treatment, indicating that terpinen-4-ol-elicited apoptosis is p53-dependent. Moreover, intratumoral administration of terpinen-4-ol significantly suppressed the growth of s.c. A549 xenografts by inducing apoptosis, as confirmed by TUNEL assay. Collectively, these data provide insight into the molecular mechanisms underlying terpinen-4-ol-induced apoptosis in NSCLC cells, rendering this compound a potential anticancer drug for NSCLC.

scholarly journals Digoxin exerts anticancer activity on human nonsmall cell lung cancer cells by blocking PI3K/Akt pathway

2021 ◽  
Vol 41 (10) ◽  
Author(s):  
Yingying Wang ◽  
Yongqiang Hou ◽  
Lanjiao Hou ◽  
Wei Wang ◽  
Ke Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Nonsmall Cell Lung Cancer ◽  
Metastatic Potential ◽  
Akt Pathway ◽  
Mesenchymal Transition ◽  
M Phase

Abstract Lung cancer remains the leading cause of cancer mortality because of its metastatic potential and high malignancy. The discovery of new applications for old drugs is a shortcut for cancer therapy. We recently investigated the antitumor effect of digoxin, a well-established drug for treating heart failure, against nonsmall cell lung cancer A549 and H1299 cells. Digoxin inhibited the proliferation and colony-forming ability of the two cell lines and arrested the cell cycle at the G0/G1 phase in A549 cells and the G2/M phase in H1299 cells. Mitochondria-mediated apoptosis was induced in A549 cells but not in H1299 cells after treatment with digoxin. Moreover, digoxin inhibited the migration, invasion, adhesion and epithelial–mesenchymal transition of A549 and H1299 cells. Autophagy was induced in both cell lines after treatment with digoxin, with an increase in autophagosome foci. In addition, digoxin inhibited the phosphorylation of Akt, mTOR and p70S6K, signaling molecules of the PI3K/Akt pathway that are known to be involved in tumor cell survival, proliferation, metastasis and autophagy. Our findings suggest that digoxin has the potential to be used for therapy for human nonsmall cell lung cancer, but further evidence is required.

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