Sulforaphene–Carboplatin Combination Synergistically Enhances Apoptosis by Disruption of Mitochondrial Membrane Potential and Cell Cycle Arrest in Human Non-Small Cell Lung Carcinoma

2016 ◽  
Vol 19 (9) ◽  
pp. 860-869 ◽  
Author(s):  
Saswata Chatterjee ◽  
Yun-Hee Rhee ◽  
Jin-Chul Ahn
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Cell Cycle Arrest ◽  
Lung Carcinoma ◽  
Mitochondrial Membrane ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cycle Arrest

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 Alantolactone pyrazoline analogue inhibits cancer cell proliferation and induces apoptosis in non-small cell lung carcinoma cells

2015 ◽  
Vol 10 (2) ◽  
pp. 409 ◽  
Author(s):  
Jing Lv ◽  
Ming-Qin Cao ◽  
Jian-Chun Yu
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Chromatin Condensation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cycle Arrest ◽  
H460 Cells ◽  
Dose Dependent

<p>The aim of the current study was to evaluate the anticancer and apoptotic effects of alantolactone pyrazoline analogue in human non-small cell lung cancer (NCI-H460) cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide) assay was used to evaluate the cell viability while as fluorescence microscopy was used to assess the effect on apoptosis, cellular and nuclear morphology. Flow cytometry evaluated the effect of APA on cell cycle arrest in these cells. The results revealed that APA induced potent, time and dose-dependent cytotoxic effects on the growth of NCI-H460 cells. It also inhibited colony forming tendency as well as cell invasion capability of these cancer cells. APA induced dose-dependent nuclear and cellular morphological effects including chromatin condensation and DNA fragmentation. Flow cytometry revealed that the anticancer effects of APA might be due to its cell cycle arrest inducing tendency in G0/G1 phase of the cell cycle.</p>

scholarly journals Toxoplasma GRA16 Inhibits NF-κB Activation through PP2A-B55 Upregulation in Non-Small-Cell Lung Carcinoma Cells

2020 ◽  
Vol 21 (18) ◽  
pp. 6642
Author(s):  
Seung-Hwan Seo ◽  
Sang-Gyun Kim ◽  
Ji-Hun Shin ◽  
Do-Won Ham ◽  
Eun-Hee Shin
Keyword(s):  
Cell Cycle ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Xenograft Model ◽  
Cyclin B1 ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Anticancer Effects ◽  
Mouse Xenograft Model

Nuclear factor kappa B (NF-κB) activation is a well-known mechanism by which chemoresistance to anticancer agents is reported. It is well-known that irinotecan as a chemotherapeutic drug against non-small-cell lung carcinoma (NSCLC) has limited anticancer effect due to NF-κB activation. In this study, we propose the novel role of GRA16, a dense granule protein of Toxoplasma gondii, as an anticancer agent to increase the effectiveness of chemotherapy via the inhibition of NF-κB activation. To demonstrate this, H1299 cells were stably transfected with GRA16. The anticancer effects of GRA16 were demonstrated as a reduction in tumor size in a mouse xenograft model. GRA16 directly elevated B55 regulatory subunit of protein phosphatase 2A (PP2A-B55) expression in tumor cells, thereby decreasing GWL protein levels and ENSA phosphorylation. This cascade, in turn, induced PP2A-B55 activation and suppressed AKT/ERK phosphorylation and cyclin B1 levels, suggesting reduced cell survival and arrested cell cycle. Moreover, PP2A-B55 activation and AKT phosphorylation inhibition led to NF-κB inactivation via the reduction in inhibitory kappa B kinase beta (IKKβ) levels, de-phosphorylation of inhibitor of kappa B alpha (IκBα), and reduction in the nuclear transit of NF-κB p65. Furthermore, this molecular mechanism was examined under irinotecan treatment. The PP2A-B55/AKT/NF-κB p65 pathway-mediated anticancer effects were only induced in the presence of GRA16, but not in the presence of irinotecan. Moreover, GRA16 synergistically promoted the anticancer effects of irinotecan via the induction of the sub-G1 phase and reduction of cell proliferation. Collectively, irinotecan and GRA16 co-treatment promotes the anticancer effects of irinotecan via NF-κB inhibition and cell cycle arrest induced by GRA16, subsequently increasing the chemotherapeutic effect of irinotecan to NSCLC cells via NF-κB inhibition.

Gender and smoking differences in cell cycle marker expressions and p-TNM stage in non-small cell lung carcinoma

2010 ◽  
Vol 4 (1) ◽  
pp. 1-8
Author(s):  
Yong-Beom Kim ◽  
Dong Wook Kang ◽  
Hyunjung Lee ◽  
Min-Kyung Yeo ◽  
Mi-Ran Kim ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Tnm Stage ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

Histologic-Type Specific Role of Cell Cycle Regulators in Non-Small Cell Lung Carcinoma

2010 ◽  
Vol 164 (2) ◽  
pp. 256-265 ◽  
Author(s):  
Vassiliki G. Zolota ◽  
Vassiliki N. Tzelepi ◽  
Michael Leotsinidis ◽  
Paraskevi E. Zili ◽  
Nikolaos D. Panagopoulos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Lung Carcinoma ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Specific Role ◽  
Histologic Type ◽  
Cell Cycle Regulators ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma
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