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Inhibitory Effect of High Concentration Insulin on K562 Cell Proliferation and Its Mechanism / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 411-415, 2016.
Artigo em Chinês | WPRIM | ID: wpr-360076
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the inhibitory effect of high concentration insulin on K562 cell proliferation and its underlying mechanism.</p><p><b>METHODS</b>K562 cells were treated by different concentration of insulin and/or anti-IGF-1R antibody (IGF-1R-Ab), MTT assay and flow cytometry were used to detect the K562 cells proliferation and apoptosis, respectivety; Western blot was used to measure the expression and phosphorylation level of IGE-IR, Akt, Erk1/2 in K562 cells under the different concentration of insulin.</p><p><b>RESULTS</b>MTT assay showed that less than 40 mU/ml insulin could promote K562 cell proliferation, while high concentration (> 40 mU/ml) insulin has been shown to inhibit K562 cell proliferation; Flow cytometry showed that 40 mU/ml insulin suppressed K562 cell apoptosis (P < 0.05), while 200 mU/ml insulin could significantly induce K562 cell apoptosis (P < 0.01); 0.01 to 1.0 µg/ml IGF-1R-Ab has significantly enhanced the inhibitory and inducing effects of high concentration (> 40 mU/ml) of insulin on K562 cell proliferation and apoptosis respectively (r = 0.962, P < 0.001); Western blot showed that after K562 cells were treated with different concentrations of insulin ERK, and the p-ERK expression did not change significantly, after K562 cells were treated with 200 mU/ml insulin, the expression of IGF-1R and AKT also not were changed obviously, while the phosphorylation level of IGF-1R and AKT increased.</p><p><b>CONCLUSION</b>High concentration (>40 mU/ml) of insulin inhibits K562 cell proliferation and induces its apoptosis, and its mechanism may be related with the binding IGF-1R by insulin, competitively inhibiting the binding of IGF-1 and IGF-1R, the blocking the transduction of PI3K/AKT signal pathway.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Fosforilação / Fator de Crescimento Insulin-Like I / Transdução de Sinais / Química / Receptores de Somatomedina / Apoptose / Fosfatidilinositol 3-Quinases / Células K562 / Meios de Cultura Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Farmacologia / Fosforilação / Fator de Crescimento Insulin-Like I / Transdução de Sinais / Química / Receptores de Somatomedina / Apoptose / Fosfatidilinositol 3-Quinases / Células K562 / Meios de Cultura Limite: Humanos Idioma: Chinês Revista: Journal of Experimental Hematology Ano de publicação: 2016 Tipo de documento: Artigo