scholarly journals Pomegranate Juice Induced Cell Cycle Arrest and Apoptosis Via Mitochondrial Pathway in Human Lung Aden carcinoma A549 Cells

2018 ◽  
Vol 7 (3.21) ◽  
pp. 287
Author(s):  
Radiah Abdul Ghani ◽  
Nik Nurasyikin Nik Abdul Malek ◽  
Noor Suryani Mohd Ashari ◽  
Norzamzila Abdullah
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
A549 Cells ◽  
Mitochondrial Pathway ◽  
Pomegranate Juice ◽  
Mitochondrial Membrane Permeability ◽  
Cycle Arrest

Lung cancer is the most common type of cancer which the mortality rate increases year by year. Therapeutic drugs could not control the progression of cancer and it contributes to the side effects in normal cells. Thus, an alternative strategy using natural product becomes a focus today. Punica granatum, known as pomegranate  has demonstrated the anti-proliferative effect in A549 cells. To further confirm its efficacy, this study aimed to investigate the type of cell death and its pathway in A549 cells. Propium Iodide staining was applied to determine the cell cycle profile changes induced by this juice. The determination of type of cell death was done using Annex in-V staining and later will be analyzed using flow cytometer. The pathway to apoptosis was investigated by determining the caspase- 3, 8 and 9 activities. The findings were supported by mitochondrial membrane permeability assay and cytochrome c release detection which were later analyzed using flow cytometer. This study revealed that pomegranate juice induced cell cycle arrest at G0/G1 phase and apoptosis through intrinsic pathway following 24 h treatment. Pomegranate juice caused loss of mitochondrial membrane permeability after 48 h (p<0.05) exposure and a release of cytochrome c in cytosol after 24 h (p<0.05) and 48 h (p<0.01) exposure in treated A549 cells. In caspases analysis, it was showed that there was activation of caspase-3 following 72 h (p<0.01) treatment and caspase-9 after 48 (p<0.01) and 72 h (p<0.05) exposure in treated A549 cells. It can be concluded that pomegranate juice able to cause A549 cell growth inhibition by inducing cell cycle arrest and apoptosis through mitochondrial pathway. 

scholarly journals Pomegranate Juice Induced Cell Cycle Arrest and Apoptosis via Mitochondrial Pathway in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 7 (3.30) ◽  
pp. 309
Author(s):  
Radiah Abdul Ghani ◽  
Nik Nurasyikin Nik Abdul Malek ◽  
Norzamzila Abdullah
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
A549 Cells ◽  
Mitochondrial Pathway ◽  
Pomegranate Juice ◽  
Mitochondrial Membrane Permeability ◽  
Cycle Arrest

Lung cancer is the most common type of cancer which the mortality rate increases year by year. Therapeutic drugs could not control the progression of cancer and it contributes to the side effects in normal cells. Thus, an alternative strategy using natural product becomes a focus today. Punica granatum, known as pomegranate has demonstrated the anti-proliferative effect in A549 cells. To further confirm its efficacy, this study aimed to investigate the type of cell death and its pathway in A549 cells. Propium Iodide staining was applied to determine the cell cycle profile changes induced by this juice. The determination of type of cell death was done using Annexin-V staining and later will be analysed using flowcytometer. The pathway to apoptosis was investigated by determining the caspase- 3, 8 and 9 activities. The findings were supported by mitochondrial membrane permeability assay and cytochrome c release detection which were later analysed using flowcytometer. This study revealed that pomegranate juice induced cell cycle arrest at G0/G1 phase and apoptosis through intrinsic pathway following 24 h treatment. Pomegranate juice caused loss of mitochondrial membrane permeability after 48 h [p<0.05] exposure and a release of cytochrome c in cytosol after 24 h [p<0.05] and 48 h [p<0.01] exposure in treated A549 cells. In caspases analysis, it was showed that there was activation of caspase-3 following 72 h [p<0.01] treatment and caspase-9 after 48 [p<0.01] and 72 h [p<0.05] exposure in treated A549 cells. It can be concluded that pomegranate juice able to cause A549 cell growth inhibition by inducing cell cycle arrest and apoptosis through mitochondrial pathway. 

Effects of 5,6-Dihydroxy-2,4-Dimethoxy-9,10-Dihydrophenanthrene on G2/M Cell Cycle Arrest and Apoptosis in Human Lung Carcinoma Cells

2016 ◽  
Vol 44 (07) ◽  
pp. 1473-1490 ◽  
Author(s):  
Wipada Duangprompo ◽  
Kalaya Aree ◽  
Arunporn Itharat ◽  
Pintusorn Hansakul
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Human Lung ◽  
A549 Cells ◽  
Human Lung Cancer ◽  
Apoptotic Cells ◽  
Mrna Levels ◽  
Cycle Arrest

5,6-dihydroxy-2,4-dimethoxy-9,10-dihydrophenanthrene (HMP) is an active compound isolated from the rhizome extracts of Dioscorea membranacea Pierre, a Thai medicinal plant. This study aimed to investigate the growth-inhibitory and apoptosis-inducing effects of HMP in human lung cancer A549 cells. The antiproliferative and cytotoxic effects of HMP were analyzed by a Sulforhodamine B assay. Cell division, cell cycle distribution and membrane asymmetry changes were each performed with different fluorescent dyes and then analyzed by flow cytometry. Real-time PCR and immunoblotting were used to detect cell cycle- and apoptosis-related mRNA levels and proteins, respectively. The nuclear morphology of the cells stained with DAPI and DNA fragmentation were detected by fluorescence microscopy and gel electrophoresis, respectively. The results showed that HMP exerted strong antiproliferative and cytotoxic activities in A549 cells with the highest selectivity index. It halted the cell cycle in [Formula: see text]/M phase via down-regulation of the expression levels of regulatory proteins Cdc25C, Cdk1 and cyclinB1. In addition, HMP induced early apoptotic cells with externalized phosphatidylserine and subsequent apoptotic cells in sub-[Formula: see text] phase. HMP increased caspase-3 activity and levels of the cleaved (active) form of caspase-3 whose actions were supported by the cleavage of its target PARP, nuclear condensation and DNA apoptotic ladder. Moreover, HMP significantly increased the mRNA and protein levels of proapoptotic Bax as well as promoted subsequent caspase-9 activation and BID cleavage, indicating HMP-induced apoptosis via both intrinsic and extrinsic pathways. These data support, for the first time, the potential role of HMP as a cell-cycle arrest and apoptosis-inducing agent for lung cancer treatment.

Propylparaben induces apoptotic cell death in human placental BeWo cells via cell cycle arrest and enhanced caspase-3 activity

2019 ◽  
Vol 16 (1) ◽  
pp. 83-92 ◽  
Author(s):  
Mi Jin Kim ◽  
Chul-Hong Kim ◽  
Mi-Jin An ◽  
Ju-Hyun Lee ◽  
Geun-Seup Shin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Bewo Cells ◽  
Cycle Arrest

Paris Saponin VII Induces Apoptosis and Cell Cycle Arrest in Erythroleukemia Cells by a Mitochondrial Membrane Signaling Pathway

2020 ◽  
Vol 20 ◽  
Author(s):  
Xin Lin ◽  
Babu Gajendran ◽  
Krishnapriya M. Varier ◽  
Wuling Liu ◽  
Jingrui Song ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Mtt Assay ◽  
Mitochondrial Membrane ◽  
Antimicrobial Activities ◽  
Mitochondrial Pathway ◽  
S Phase ◽  
Phase Cell ◽  
Cycle Arrest ◽  
Hel Cells

Background and Purpose: Leukemia considered a top-listed ailment, according to WHO, which contributes to the death of a major population of the world every year. Paris Saponin VII (PS), a saponin which was isolated from the roots of Trillium kamtschaticum, from our group, was reported to provide hemostatic, cytotoxic and antimicrobial activities. However, its molecular mechanism underlying the anti-proliferative effects remains unclear. Thus, this study hypothesized to assess that mechanism in PS treated HEL cells. Methods: The MTT assay used to analyze the PS inhibited cell viability in the HEL cells. We further found that PS could induce S phase cell cycle arrest through flow cytometry as well as the western blot analysis of intrinsic and extrinsic apoptotic molecules. Results: The MTT assay showed the IC50 concentration of PS as 0.667μM. The study revealed that PS treatment inhibits cell proliferation dose-dependently. It further caused mitochondrial membrane potential changes by PS treatment. Mechanistic protein expression revealed a dose-dependent upsurge for Bid and Bim molecules, while Bcl2 and PARP expression levels were significantly (P< 0.05) down-regulated in PS treated HEL cells resulting in caspase -3 release and increased the Bim levels upon 24h of incubation. Conclusions: These findings indicate that PS possesses an excellent anti-leukemic activity via regulation of the mitochondrial pathway, leading to S phase cell cycle arrest and caspase-dependent apoptosis suggesting it as a potential alternative chemotherapeutic agent for leukemia patients.

Retraction: A Dihydrobenzofuran Lignan Induces Cell Death by Modulating Mitochondrial Pathway and G2/M Cell Cycle Arrest

2013 ◽  
Vol 56 (4) ◽  
pp. 1787-1787
Author(s):  
Julie S. Bose ◽  
Vijay Gangan ◽  
Ravi Prakash ◽  
Swatantra Kumar Jain ◽  
Sunil Kumar Manna
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Mitochondrial Pathway ◽  
M Cell ◽  
Cycle Arrest

A Dihydrobenzofuran Lignan Induces Cell Death by Modulating Mitochondrial Pathway and G2/M Cell Cycle Arrest

2009 ◽  
Vol 52 (10) ◽  
pp. 3184-3190 ◽  
Author(s):  
Julie S. Bose ◽  
Vijay Gangan ◽  
Ravi Prakash ◽  
Swatantra Kumar Jain ◽  
Sunil Kumar Manna
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Mitochondrial Pathway ◽  
M Cell ◽  
Cycle Arrest

3, 3-Dimethylquercetin Inhibits the Proliferation of Human Colon Cancer RKO Cells through Inducing G2/M Cell Cycle Arrest and Apoptosis

2019 ◽  
Vol 19 (3) ◽  
pp. 402-409 ◽  
Author(s):  
Jianguo Wu ◽  
Jun Yi ◽  
Yanbin Wu ◽  
Xuzheng Chen ◽  
Jianwei Zeng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Membrane Potential ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Human Colon ◽  
Caspase 9 ◽  
Human Colon Cancer ◽  
Cycle Arrest

Background: Our previous study successfully identified that 3,3-Dimethylquercetin (DMQ) acted as a potent anticancer agent against human colon cancer cell lines RKO. Thus, this study was conducted to investigate the underlying mechanism by which DMQ displayed inhibitory activity in RKO cells. Methods: Flow cytometry was used to evaluate the effect of DMQ on the cell cycle arrest, as well as the mitochondrial membrane potential in RKO cells. DAPI staining and DNA fragmentation ladder assays were performed to assess the apoptosis inducing activity of DMQ. Furthermore, western blot analysis was conducted to examine the expression of related proteins responsible for the cell cycle arrest and apoptosis. Results: Treatment with DMQ caused a significant increase in the fraction of G2/M cells, and induced remarkable apoptosis. Furthermore, western blot analysis showed that DMQ arrested cells at G2/M checkpoint by down-regulation of cyclin B1, cdc2 and cdc25c and up-regulation of p21, and induced cell apoptosis via affecting the ratio of Bax/Bcl-2, causing loss of the mitochondrial membrane potential and enhancing the expression of cleaved caspase-9 (C-caspase-9) and cleaved caspase-3 (C-caspase-3). Conclusion: These data showed that DMQ could suppress RKO cell growth by arresting RKO cells at G2/M checkpoint and inducing mitochondria-dependent cell apoptosis. Our findings shed light on the potential use of DMQ as a chemotherapeutic agent for CRC.

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