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Chinese Journal of Pathology ; (12): 95-99, 2010.
Artigo em Chinês | WPRIM | ID: wpr-273449

RESUMO

<p><b>OBJECTIVE</b>To investigate the status of Notch signaling pathway in small cell lung cancer (SCLC).</p><p><b>METHODS</b>Expression plasmids of pEFBOS-NIC-MYC and pEFBOS-neo were transfected into NCI-H446 cells. Stably transfected cell lines were selected and their growth rates were examined by MTT method. Expression of downstream genes along the Notch signaling pathway were studied by RT-PCR. Protein expression of euroendocrine markers of CgA and NSE were detected by Western blot analysis and immunocytochemistry.</p><p><b>RESULTS</b>The expression of HES1 was increased in the pEFBOS-NIC-MYC group, but the expression of hASH in the pEFBOS-NIC-MYC group was decreased significantly. The transfected cells with pEFBOS-NIC-MYC plasmid showed a significantly slower growth rate compared with that of two control groups (P < 0.05, Student's t-test). Immunocytochemistry of NSE showed that PUs in the NIC transfected group, sham group and negative control group were 7.21 ± 0.59, 28.25 ± 1.46, 30.57 ± 1.31 respectively, the former one was smaller than the values of the latter two significantly (P < 0.01). Western blot analysis showed the grave scales of CgA in NIC transfected group and sham group to be 0.54 ± 0.03 and 0.99 ± 0.05 respectively (grave scales of the negative control was set as 1.00), the former one significantly smaller than that of the other two groups (P < 0.01). The grave scales of NSE in the NIC transfected group and sham group were 0.43 ± 0.02 and 1.07 ± 0.09 respectively (grave scales of the negative control was set as 1.00) and the former one was significantly smaller than the other two groups (P < 0.01).</p><p><b>CONCLUSION</b>Notch signaling pathway regulates SCLC cells through its inhibitory effect on hASH1 transcription via HES1 along with an expression inhibition of neuroendocrine markers in SCLC.</p>


Assuntos
Humanos , Fatores de Transcrição Hélice-Alça-Hélice Básicos , Metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Cromogranina A , Metabolismo , Proteínas de Homeodomínio , Metabolismo , Neoplasias Pulmonares , Metabolismo , Patologia , Fosfopiruvato Hidratase , Metabolismo , Plasmídeos , Receptor Notch1 , Metabolismo , Fisiologia , Proteínas Recombinantes , Metabolismo , Transdução de Sinais , Carcinoma de Pequenas Células do Pulmão , Metabolismo , Patologia , Fatores de Transcrição HES-1 , Transfecção
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