scholarly journals Apoptosis Induction byPolygonum minusIs Related to Antioxidant Capacity, Alterations in Expression of Apoptotic-Related Genes, and S-Phase Cell Cycle Arrest in HepG2 Cell Line

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Mohd Alfazari Mohd Ghazali ◽  
Ghanya Al-Naqeb ◽  
Kesavanarayanan Krishnan Selvarajan ◽  
Mizaton Hazizul Hasan ◽  
Aishah Adam
Keyword(s):  
Cell Cycle ◽  
Ethyl Acetate ◽  
Antioxidant Capacity ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
S Phase ◽  
Antiproliferative Effect ◽  
Phase Cell ◽  
Apoptosis Induction ◽  
Cycle Arrest

Polygonum minus(Polygonaceae) is a medicinal herb distributed throughout eastern Asia. The present study investigated antiproliferative effect ofP. minusand its possible mechanisms. Four extracts (petroleum ether, methanol, ethyl acetate, and water) were prepared by cold maceration. Extracts were subjected to phytochemical screening, antioxidant, and antiproliferative assays; the most bioactive was fractionated using vacuum liquid chromatography into seven fractions (F1–F7). Antioxidant activity was measuredviatotal phenolic content (TPC), 2,2-diphenyl-1-picrylhydrazyl (DPPH), and ferric reducing antioxidant power (FRAP) assays. Antiproliferative activity was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Most active fraction was tested for apoptosis induction and cell cycle arrest in HepG2 cells using flow cytometry and confocal microscopy. Apoptotic-related gene expression was studied by RT-PCR. Ethyl acetate extract was bioactive in initial assays. Its fraction, F7, exhibited highest antioxidant capacity (TPC;113.16±6.2 mg GAE/g extract, DPPH;EC50:30.5±3.2 μg/mL, FRAP;1169±20.3 μmol Fe (II)/mg extract) and selective antiproliferative effect (IC50:25.75±1.5 μg/mL). F7 induced apoptosis in concentration- and time-dependent manner and caused cell cycle arrest at S-phase. Upregulation of proapoptotic genes (Bax,p53, andcaspase-3) and downregulation of antiapoptotic gene,Bcl-2, were observed. In conclusion, F7 was antiproliferative to HepG2 cells by inducing apoptosis, cell cycle arrest, andviaantioxidative effects.

scholarly journals Cannabisin B induces autophagic cell death by inhibiting the AKT/mTOR pathway and S phase cell cycle arrest in HepG2 cells

2013 ◽  
Vol 138 (2-3) ◽  
pp. 1034-1041 ◽  
Author(s):  
Tianpeng Chen ◽  
Jianxiong Hao ◽  
Jinfeng He ◽  
Jianchun Zhang ◽  
Yingcong Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
S Phase ◽  
Mtor Pathway ◽  
Autophagic Cell Death ◽  
Phase Cell ◽  
Cycle Arrest

Involvement of the p38 MAPK signaling pathway in S-phase cell-cycle arrest induced by Furazolidone in human hepatoma G2 cells

2012 ◽  
Vol 33 (12) ◽  
pp. 1500-1505 ◽  
Author(s):  
Yu Sun ◽  
Shusheng Tang ◽  
Xi Jin ◽  
Chaoming Zhang ◽  
Wenxia Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
S Phase ◽  
Mapk Signaling Pathway ◽  
Phase Cell ◽  
Human Hepatoma ◽  
Cycle Arrest

Ciprofloxacin-mediated induction of S-phase cell cycle arrest and apoptosis in COLO829 melanoma cells

2018 ◽  
Vol 70 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Artur Beberok ◽  
Dorota Wrześniok ◽  
Aldona Minecka ◽  
Jakub Rok ◽  
Marcin Delijewski ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Melanoma Cells ◽  
S Phase ◽  
Phase Cell ◽  
Cycle Arrest

scholarly journals Potent organometallic osmium compounds induce mitochondria-mediated apoptosis and S-phase cell cycle arrest in A549 non-small cell lung cancer cells

Metallomics ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 1014 ◽  
Author(s):  
Sabine H. van Rijt ◽  
Isolda Romero-Canelón ◽  
Ying Fu ◽  
Steve D. Shnyder ◽  
Peter J. Sadler
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Small Cell ◽  
S Phase ◽  
Phase Cell ◽  
Small Cell Lung ◽  
Cycle Arrest

scholarly journals Ghrelin enhances cisplatin sensitivity in HO-8910 PM human ovarian cancer cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yun Leng ◽  
Can Zhao ◽  
Guoliang Yan ◽  
Shuangyue Xu ◽  
Yinggui Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cyclin B1 ◽  
Inhibitory Effect ◽  
S Phase ◽  
Phase Cell ◽  
Ovarian Cancer Cells ◽  
Cycle Arrest

Abstract Background Resistance to platinum-based chemotherapy is one of the crucial problems in ovarian cancer treatment. Ghrelin, a widely distributed peptide hormone, participates in a series of cancer progression. The aim of this study is to determine whether ghrelin influences the sensitivity of ovarian cancer to cisplatin, and to demonstrate the underlying mechanism. Methods The anti-tumor effects of ghrelin and cisplatin were evaluated with human ovarian cancer cells HO-8910 PM in vitro or in vivo. Cell apoptosis and cell cycle were analyzed via flow cytometry assay. The signaling pathway and the expression of cell cycle protein were analyzed with Western Blot. Results Our results showed that treatment with ghrelin specifically inhibited cell proliferation of HO-8910 PM and sensitized these cells to cisplatin via S phase cell cycle arrest, and enhanced the inhibitory effect of cisplatin on tumor growth of HO-8910 PM derived xenografts in vivo. Treatment with ghrelin inhibited the expression of p-Erk1/2 and p-p38, which was opposite the effect of cisplatin. However, under the treatment of ghrelin, cisplatin treatment exhibited a stronger effect on inhibiting P21 expression, upregulating p-CDK1 and cyclin B1 expression, and blocking cell cycle progression. Mechanistically, ghrelin promoted S phase cell cycle arrest and upregulated p-CDK1 and cyclin B1 expression induced by cisplatin via inhibition of p38. Conclusion This study revealed a specifically inhibitory effect of ghrelin on platinum-resistance via suppressing p-P38 and subsequently promoting p-CDK1 mediated cell cycle arrest in HO-8910 PM.

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