Adiponectin and colon cancer: evidence for inhibitory effects on viability and migration of human colorectal cell lines

被引:39
作者
Nigro, E. [1 ,2 ]
Schettino, P. [3 ]
Polito, R. [1 ,4 ]
Scudiero, O. [1 ,5 ]
Monaco, M. L. [1 ]
De Palma, G. D. [3 ]
Daniele, A. [1 ,4 ]
机构
[1] CEINGE Biotecnol Avanzate Scarl, Via G Salvatore 486, I-80145 Naples, Italy
[2] Univ Molise, Dipartimento Med & Sci Salute, I-86100 Campobasso, Italy
[3] Univ Napoli Federico II, Dipartimento Med Clin & Chirurg, Via S Pansini 5, I-80131 Naples, Italy
[4] Univ Campania Luigi Vanvitelli, Dipartimento Sci & Tecnol Ambientali Biol Farmace, Via G Vivaldi 42, I-81100 Caserta, Italy
[5] Univ Napoli Federico II, Dipartimento Med Mol & Biotecnol Med, Via S Pansini 5, I-80131 Naples, Italy
关键词
Adiponectin; Colorectal cancer; Cell proliferation and apoptosis; Migration; Cytokines; PROLIFERATION; OBESITY; EXPRESSION; ADIPOKINES; PATHWAY; DISEASE; GROWTH;
D O I
10.1007/s11010-018-3319-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Adiponectin (Acrp30) is an adipokine widely studied for its beneficial metabolic and anti-inflammatory properties. Colorectal cancer is among the most common cancers worldwide. The aim of present study was to explore the effects of Acrp30 on both CaCo-2 and HCT116 colorectal cancer cells in terms of viability, oxidative stress, and apoptosis. In addition, since colorectal cancer represents a typical inflammation-related cancer, we investigated whether Acrp30 treatment modifies the migration and the expression of crucial proteins in the EMT transition. Finally, we analyzed the expression of cytokines in CaCo-2 cells. We found that Acrp30 reduces the survival rate of both CaCo-2 and HCT116 cells through induction of apoptosis and oxidative stress already after 24 h of treatment. In addition, wound-healing assay indicated that Acrp30 exposure statistically inhibits CaCo-2 and HCT116 cell migration. Western blot analysis performed on E-cadherin and vimentin, two EMT crucial markers in carcinogenesis, indicated that Acrp30 does not influence EMT transition. Finally, we found a reduction of mRNA levels corresponding to the anti-inflammatory IL-10 cytokine together with an increase of the pro-inflammatory IL-6 and IL-8 cytokines. This study provides new insight into Acrp30 molecular effects on colorectal cancer cells. Indeed, even if further studies are necessary to clarify the precise role of Acrp30 in colorectal cancer, our data strongly suggest that Acrp30 negatively regulates cell survival and migration in association with induction of oxidative stress and regulation of cytokines expression in both CaCo-2 and HCT116 colorectal cells.
引用
收藏
页码:125 / 135
页数:11
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