Adiponectin as Novel Regulator of Cell Proliferation in Human Glioblastoma

被引:23
作者
Porcile, Carola [1 ]
Di Zazzo, Erika [1 ]
Monaco, Maria Ludovica [2 ,3 ]
D'Angelo, Giorgia [1 ]
Passarella, Daniela [1 ]
Russo, Claudio [1 ]
Di Costanzo, Alfonso [1 ]
Pattarozzi, Alessandra [4 ,5 ]
Gatti, Monica [4 ,5 ]
Bajetto, Adriana [4 ,5 ]
Zona, Gianluigi [6 ]
Barbieri, Federica [4 ,5 ]
Oriani, Giovannangelo [1 ,2 ]
Moncharmont, Bruno [1 ]
Florio, Tullio [4 ,5 ]
Daniele, Aurora [2 ,3 ,7 ]
机构
[1] Univ Molise, Dept Med & Hlth Sci, Campobasso, Italy
[2] CEINGE Adv Biotechnol Scarl, Naples, Italy
[3] IRCCS Fdn SDN, Naples, Italy
[4] Univ Genoa, Dept Internal Med, Pharmacol Sect, I-16126 Genoa, Italy
[5] Univ Genoa, CEBR, I-16126 Genoa, Italy
[6] IRCCS Azienda Osped Univ San Martino, Ist Nazl Ric Canc, Genoa, Italy
[7] Univ Naples 2, Dept Environm Sci, Caserta, Italy
关键词
LEPTIN GENE-EXPRESSION; COLORECTAL-CANCER; GLIOMA-CELLS; BRAIN-TUMORS; RECEPTOR; GROWTH; INHIBITION; INVOLVEMENT; MODULATION; ACTIVATION;
D O I
10.1002/jcp.24582
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Adiponectin (Acrp30) is an adipocyte-secreted hormone with pleiotropic metabolic effects, whose reduced levels were related to development and progression of several malignancies. We looked at the presence of Acrp30 receptors in human glioblastomas (GBM), hypothesizing a role for Acrp30 also in this untreatable cancer. Here we demonstrate that human GBM express Acrp30 receptors (AdipoR1 and AdipoR2), which are often co-expressed in GBM samples (70% of the analyzed tumors). To investigate the effects of Acrp30 on GBM growth, we used human GBM cell lines U87-MG and U251, expressing both AdipoR1 and AdipoR2 receptors. In these cells, Acrp30 treatment inhibits DNA synthesis and cell proliferation rate, inducing arrest in G1 phase of the cell cycle. These effects were correlated to a sustained activation of ERK1/2 and Akt kinases, upon Acrp30 treatment. Our results suggest that Acrp30 may represent a novel endogenous negative regulator of GBM cell proliferation, to be evaluated for the possible development of novel pharmacological approaches. (C) 2014 Wiley Periodicals, Inc.
引用
收藏
页码:1444 / 1454
页数:11
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