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Somatostatin receptor 1,2 and 5 activation leads to C6 glioma growth arrest in vitro and in vivo; analysis of the intracellular pathways involved
Author(s) -
Monica Gatti,
Alessandra Pattarozzi,
Roberto Würth,
Francesca Angeletti,
Federica Barbieri,
Tullio Florio
Publication year - 2011
Publication title -
journal of biological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.218
H-Index - 6
eISSN - 2284-0230
pISSN - 1826-8838
DOI - 10.4081/jbr.2011.4649
Subject(s) - in vivo , dephosphorylation , somatostatin receptor , in vitro , agonist , cancer research , somatostatin , intracellular , cell growth , somatostatin receptor 2 , microbiology and biotechnology , receptor , biology , chemistry , endocrinology , phosphorylation , biochemistry , phosphatase
We report that somatostain receptor (SSTR) 1,2 and 5 activation by selective agonista, cause C6 cell growth arrest through PTPn-dependent dephosphorylation of ERK1/2 in vitro and after xenografting in nude mice. Individual SSTR agonist desplayed different efficacy and potecy showing partial synergism by combined treatment. Since most tumor cells express multiple SSTRs, the activtion of all the subtypes may grant a better control of cancer growth

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