瘦素诱导乳腺癌细胞的凋亡抵抗及其分子机制 |
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引用本文: | 赵天锁,姜海平,王秀超,任贺,郝继辉. 瘦素诱导乳腺癌细胞的凋亡抵抗及其分子机制[J]. 中华肿瘤杂志, 2009, 31(7): 651-654. DOI: 10.3760/cma.j.issn.0253-3766.2009.09.003 |
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作者姓名: | 赵天锁 姜海平 王秀超 任贺 郝继辉 |
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作者单位: | 乳腺癌防治国家重点实验室天津医科大学附属肿瘤医院中心实验室,300060;青岛大学医学院附属医院放射科; |
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摘 要: | Objective To explore the apoptosis resistance induced by Leptin and its mechanism in breast cancer cells in vitro.Methods The leptin-mediated reduction of docetaxel-induced apoptosis in human breast cancer T47D cells was evaluated by TransAM ELISA,MTT and caspase-9 assay.The leptinpromoted survivin expression was analyzed by Western-blot and RT-PCR.The reversing effect of STAT3 knockdown on leptin-induced survivin upregulation was measured by Western-blot and RT-PCR.Results Leptin promoted T47D cells proliferation and the inhibitory rate was-63.6%.It reduced docetaxel-induced apoptosis in T47D cells by 31.9%.Leptin at different concentrations promoted survivin protein and mRNA expression in T47D cells.The expression of survivin mRNA was 4.6 fold compared with the T47D cells not treated with leptin(10 nmol/L).The expression of survivin mRNA in T47D cells was 0.55±0.15 fold after transfected with small interfering RNA(siRNA)of STAT3.The expression of survivin mRNA in STAT3 siRNA group and mock transfected group were 0.56±0.18 fold and 1.61±0.22 fold after treated by leptin,respectively.The survivin protein level of T47D mock transfected cells was increased after treated by leptin,but the protein level of T47D transfected with STAT3 siRNA cells were not changed significantly.Conclusion Leptin/STAT3 signaling is a novel pathway for up-regulation of survivin expression in breast cancer cells.
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关 键 词: | 瘦素 T47D细胞 凋亡 信号转导和转录激活因子3 |
Apoptosis resistance induced by leptin and its mechanism in breast cancer cells |
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