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Chinese Journal of Gastrointestinal Surgery ; (12): 168-174, 2014.
Artigo em Chinês | WPRIM | ID: wpr-239437

RESUMO

<p><b>OBJECTIVE</b>To explore the relationship between CD133(+) subsets cells in human gastric cancer (GC) and molecules of drug resistance and their sensitivity to 5-FU.</p><p><b>METHODS</b>Three gastric cancer cell lines therein KATO-III(, SGC7901 and MKN45 were sorted by immunomagnetic beads cell sorting method. Then above cell lines were further divided into un-sorted GC cells, CD133(+) subgroup and CD133(-) subgroup. The expressions of CD133, P-gp, Bax and Bcl-2 were determined by RT-PCR, Western blot and immunoflurescence. Meanwhile, the sensitivity to 5-FU of three subgroups was detected by CCK-8 Kit. The apoptosis induced by 5-FU in three subgroups was determined by Hoechst 33258.</p><p><b>RESULTS</b>Expressions of CD133 in three CD133(+) subgroups were significantly higher than those in un-sorted GC cells and CD133(-) subgroup (all P<0.05). Expressions of P-gp and Bcl-2 in the three GC cell lines were different (all P<0.05). There were significant differences of expressions of P-gp, Bcl-2 and Bax among CD133(+) cells, un-sorted GC cells and CD133(-) cells (all P<0.05). CCK-8 detection showed that CD133(-) subgroup of MKN45 GC cell line was more sensitive than CD133(+) cells to 5-FU (P<0.05). Hoechst 33258 staining showed that there were more apoptotic cells in CD133(-) subgroup as compared to other two subgroups, and the least apoptotic cells were observed in CD133(+) subgroup of MKN45 GC cell line (P<0.05). CD133 sirna was transfected into MKN45 GC cell line and could down-regulate the expressions of CD133, P-gp, Bcl-2 and p-Akt, while the expression of Bax increased (all P<0.05).</p><p><b>CONCLUSIONS</b>CD133 may contribute to the resistance of GC cells to chemotherapy drug through P-gp, Bcl-2 and Bax. PI3K/Akt signal pathway may be involved in this process.</p>


Assuntos
Humanos , Antígeno AC133 , Membro 1 da Subfamília B de Cassetes de Ligação de ATP , Antígenos CD , Metabolismo , Antineoplásicos , Farmacologia , Apoptose , Linhagem Celular Tumoral , Resistencia a Medicamentos Antineoplásicos , Fluoruracila , Glicoproteínas , Metabolismo , Peptídeos , Metabolismo , Fosfatidilinositol 3-Quinases , Proteínas Proto-Oncogênicas c-akt , RNA Interferente Pequeno , Neoplasias Gástricas , Tratamento Farmacológico , Metabolismo , Patologia , Proteína X Associada a bcl-2
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