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JCR 2016
جستجوی مقالات
پنجشنبه 30 بهمن 1404
Research in Pharmaceutical Sciences
، جلد ۱۵، شماره ۶، صفحات ۵۹۲-۶۰۱
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عنوان انگلیسی
Crocetin suppresses the growth and migration in HCT-116 human colorectal cancer cells by activating the p-38 MAPK signaling pathway
چکیده انگلیسی مقاله
Background and purpose: Crocetin is a natural antioxidant that is found in the crocus flower and Gardenia jasminoides (fruit). Previous studies have reported its anticancer activity both in vivo and in vitro . In addition, crocetin suppresses the growth and migration of human colorectal cancer cells, however, its mechanism of action remains to be elucidated. Therefore, the present study investigated the molecular mechanism of crocetin effect on colorectal cancer cells (HCT-116) in vitro . Experimental approach: HCT-116 cells were treated with different concentrations (0, 200, 400, 600, and 800 μM) of crocetin for 24 h. The cell survival rate was measured by MTT assay. Cell migration capacity was evaluated using the wound healing assay. The expression levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP-9) was monitored by RT-PCR. Phosphorylation of focal adhesion kinase (FAK) and p38 mitogen-activated protein kinase (MAPK) was determined using western blot. Findings/Results: The proliferation of HCT-116 was inhibited by crocetin at 800 μM ( P < 0.001). Crocetin prevented migration of HCT-116 cells ( P < 0.05) and suppressed VEGF and MMP-9 mRNA expression ( P < 0.001) and increased phosphorylation of p38 (MAPK; P < 0.001). However, no significant change in the phosphorylation of FAK was observed. Conclusion and implication: These data suggested that crocetin-induced growth- and migration-suppressing effects on HCT-116 cells may partially depend on the regulation of the p38 (MAPK) signaling pathway.
کلیدواژههای انگلیسی مقاله
Keywords, Crocetin,HCT-116 cells,Matrix metalloproteinase 9,p38-mitogen activated protein kinase,Vascular endothelial growth factor.
نویسندگان مقاله
| Esmaeil Khajeh
1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, I.R. Iran. 2Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, I.R. Iran.
| Yousef Rasmi
1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, I.R. Iran.
| Fatemeh Kheradmand
3Department of Pharmacology and Toxicology, Faculty of Pharmacy, Urmia University of Medical Sciences, Urmia, I.R. Iran.
| Hassan Malekinejad
4Department of Pharmacy Practice, Faculty of Pharmaceutical Sciences and Center of Excellence in Bioactive Resources for Innovative Clinical Applications, Chulalongkorn University, Bangkok, 10330 Thailand.
| Pornanong Aramwit
5Zanjan Metabolic Diseases Research Center, Zanjan University of Medical Sciences, Zanjan, I.R. Iran.
| Ehsan Saboory
6Department of Biology, Payame Noor University, Tehran, I.R. Iran.
| Behrokh Daeihassani
1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, I.R. Iran.
| Mahdieh Nasirzadeh
نشانی اینترنتی
http://rps.mui.ac.ir/index.php/jrps/article/view/2036
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