TY - JOUR
T1 - Adiponectin as novel regulator of cell proliferation in human glioblastoma
AU - Porcile, Carola
AU - Di Zazzo, Erika
AU - Monaco, Maria Ludovica
AU - D'Angelo, Giorgia
AU - Passarella, Daniela
AU - Russo, Claudio
AU - Di Costanzo, Alfonso
AU - Pattarozzi, Alessandra
AU - Gatti, Monica
AU - Bajetto, Adriana
AU - Zona, Gianluigi
AU - Barbieri, Federica
AU - Oriani, Giovannangelo
AU - Moncharmont, Bruno
AU - Florio, Tullio
AU - Daniele, Aurora
PY - 2014
Y1 - 2014
N2 - 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.
AB - 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.
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U2 - 10.1002/jcp.24582
DO - 10.1002/jcp.24582
M3 - Article
C2 - 24648185
AN - SCOPUS:84903481181
SN - 0021-9541
VL - 229
SP - 1444
EP - 1454
JO - Journal of cellular and comparative physiology
JF - Journal of cellular and comparative physiology
IS - 10
ER -