scholarly journals Inhibitory Effect of Dihydroaustrasulfone Alcohol on the Migration of Human Non-Small Cell Lung Carcinoma A549 Cells and the Antitumor Effect on a Lewis Lung Carcinoma-Bearing Tumor Model in C57BL/6J Mice

Marine Drugs ◽  
2014 ◽  
Vol 12 (1) ◽  
pp. 196-213 ◽  
Author(s):  
Shuo-Chueh Chen ◽  
Yi-Chung Chien ◽  
Chun-Hsu Pan ◽  
Jyh-Horng Sheu ◽  
Chih-Yi Chen ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Tumor Model ◽  
Inhibitory Effect ◽  
Small Cell ◽  
Lewis Lung ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

scholarly journals Actinomycin V Suppresses Human Non-Small-Cell Lung Carcinoma A549 Cells by Inducing G2/M Phase Arrest and Apoptosis via the p53-Dependent Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (10) ◽  
pp. 572 ◽  
Author(s):  
Shi-qi Lin ◽  
Fu-juan Jia ◽  
Cai-yun Zhang ◽  
Fang-yuan Liu ◽  
Jia-hui Ma ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cycle Arrest ◽  
M Phase

Actinomycin V, extracted and separated from marine-derived actinomycete Streptomyces sp., as the superior potential replacement of actinomycin D (which showed defect for its hepatotoxicity) has revealed an ideal effect in the suppression of migration and invasion in human breast cancer cells as referred to in our previous study. In this study, the involvement of p53 in the cell cycle arrest and pro-apoptotic action of actinomycin V was investigated in human non-small-cell lung carcinoma A549 cells. Results from the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay showed that cytotoxic activity of actinomycin V on A549 cells (with wild-type p53) was stronger than the NCI-H1299 cells (p53-deficient). Actinomycin V upregulated both of the protein and mRNA expression levels of p53, p21Waf1/Cip1 and Bax in A549 cells. For this situation, actinomycin V decreased the M-phase related proteins (Cdc2, Cdc25A and Cyclin B1) expression, arrested cells in G2/M phase and subsequently triggered apoptosis by mediating the Bcl-2 family proteins’ expression (Bax and Bcl-2). Furthermore, the effects of cell cycle arrest and apoptosis in A549 cells which were induced by actinomycin V could be reversed by the pifithrin-α, a specific inhibitor of p53 transcriptional activity. Collectively, our results suggest that actinomycin V causes up-regulation of p53 by which the growth of A549 cells is suppressed for cell cycle arrest and apoptosis.

scholarly journals Neuropeptide gastrin-releasing peptide induces PI3K/reactive oxygen species–dependent migration in lung adenocarcinoma cells

Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769432 ◽  
Author(s):  
Natália Jaeger ◽  
Rafael Sanguinetti Czepielewski ◽  
Maira Bagatini ◽  
Bárbara N Porto ◽  
Cristina Bonorino
Keyword(s):  
Reactive Oxygen Species ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Small Cell ◽  
Oxygen Species ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Peptide Receptor ◽  
Gastrin Releasing Peptide

Nerve fibers and neurotransmitters have increasingly been shown to have a role in tumor progression. Gastrin-releasing peptide is a neuropeptide linked to tumor aggressiveness, acting as an autocrine tumor growth factor by binding to its receptor, gastrin-releasing peptide receptor, expressed by many tumors. Although neuropeptides have been previously linked to tumor cell proliferation, more recent studies have uncovered roles for neuropeptides in chemotaxis and metastasis. Understanding the precise roles of such peptides in cancer is crucial to optimizing targeted therapy design. We have previously described that gastrin-releasing peptide acts directly as a chemotactic factor for neutrophils, dependent on PI3K, ERK, and p38. In this study, we investigated roles for gastrin-releasing peptide in lung adenocarcinoma. We asked if gastrin-releasing peptide would act as a proliferative and/or chemotactic stimulus for gastrin-releasing peptide receptor–expressing tumor cells. In A549 cells, a non-small cell lung carcinoma line, the treatment with gastrin-releasing peptide leads to activation of AKT and ERK1/2, and production of reactive oxygen species. Gastrin-releasing peptide induced migration of A549 cells, dependent on gastrin-releasing peptide receptor and PI3K, but not ERK. However, no proliferation was observed in these cells in response to gastrin-releasing peptide, and gastrin-releasing peptide did not promote resistance to treatment with a chemotherapy drug. Our results suggest that, similar to what happens in neutrophils, gastrin-releasing peptide is a migratory, rather than a proliferative, stimulus, for non–small cell lung carcinoma cells, indicating a putative role for gastrin-releasing peptide and gastrin-releasing peptide receptor in metastasis.

Targeting apoptosis by 1,2-diazole through regulation of EGFR, Bcl-2 and CDK-2 mediated signaling pathway in human non-small cell lung carcinoma A549 cells

Gene ◽  
2018 ◽  
Vol 679 ◽  
pp. 352-359 ◽  
Author(s):  
Venugopal Vinod Prabhu ◽  
Perumal Elangovan ◽  
Sivasithambaram Niranjali Devaraj ◽  
Kunnathur Murugesan Sakthivel
Keyword(s):  
Signaling Pathway ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

scholarly journals Staurosporine Induces the Generation of Polyploid Giant Cancer Cells in Non-Small-Cell Lung Carcinoma A549 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Alexander Glassmann ◽  
Carmen Carrillo Garcia ◽  
Viktor Janzen ◽  
Dominik Kraus ◽  
Nadine Veit ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Small Cell ◽  
Dependent Manner ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Inhibition Of Proliferation ◽  
Polyploid Giant Cancer Cells

Cultivation of A549 non-small-cell lung carcinoma (NSCLC) cells in the presence of staurosporine (SSP) leads to a reduction or a lack of proliferation in a concentration-dependent manner. This inhibition of proliferation is accompanied by the generation of polyploid giant cancer cells (PGCCs) that are characterized by cell flattening, increased cell size, polyploidy, and polynucleation as determined by crystal violet staining, BrdU and DiI labelling, and flow cytometry as well as video time-lapse analysis. Continuous SSP treatment of A549 cells can preserve PGCCs for at least two months in a resting state. Upon removal of SSP, A549 PGCCs restart to divide and exhibit a proliferation pattern and cellular morphology indistinguishable from cells where PGCCs originally derived from. Thus, SSP-treated A549 cells represent a simple and reliable experimental model for the reversible generation of PGCCs and their subsequent experimental analysis.

Apatinib Suppresses Biological Activities of Non-Small-Cell Lung Carcinoma(A549) Cells by Depressing miRNA-21 via the PTEN/PI3K/AKT Pathway

2019 ◽  
Vol 9 (5) ◽  
pp. 646-654
Author(s):  
Guozheng Ding ◽  
Erchun Zhang
Keyword(s):  
Wound Healing ◽  
Lung Carcinoma ◽  
Biological Activities ◽  
Small Cell Lung Carcinoma ◽  
A549 Cells ◽  
Small Cell ◽  
Akt Pathway ◽  
Control Group ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

Objective: To explain the anti-tumour effects of apatinib via the regulation of miRNA-21 in the PTEN/PI3K/AKT pathway. Methods: Measuring pathology, miRNA-21 and PTEN expression by H&E staining, in-situ hybridisation and immunohistochemistry in non-small-cell lung carcinoma (NSCLC). For the experiment, A549 cells were divided into four groups: apatinib, apatinib+blank, apatinib+miRNA and negative control. Cell proliferation, apoptosis, cell cycle, invasion and migration were assessed using the MTT, flow cytometry, transwell migration and wound-healing assays. Relative expressions of PTEN, PI3K, AKT, P21, MMP-2 and MMP-9 were evaluated using western blotting. Results: miRNA-21 and PTEN protein expressions of NSCLC tissues were found to significantly differ from those of adjacent normal tissues (P < 0.001). Compared with the control group, the cell apoptosis rate was significantly suppressed with increasing cell apoptosis in the G1 phase in the apatinib group (P < 0.001); the invasion A549 cell number and wound-healing rate were significantly depressed in the apatinib group compared with the control group (P < 0.001). However, A549 cell biological activities were significantly recovered with miRNA-21 transfection in the apatinib+miRNA group (P < 0.001). Western blotting revealed that PTEN and P21 expression in the apatinib group were significantly upregulated and that PI3K, AKT, MMP-2 and MMP-9 expression were significantly downregulated compared with the control (P < 0.001). miRNA-21 transfection led to significant suppression of PTEN and P21 expression and significant stimulation of PI3K, AKT, MMP-2 and MMP-9 expression (P < 0.001). Conclusion: Apatinib was proven to exhibit anti-tumour effects to NSCLC by regulating miRNA-21 via the PTEN/PI3K/AKT pathway.

Sign in / Sign up

Export Citation Format

Share Document