谭明旗, 孙惠梅, 边明艳. HA14-1 联合环磷酰胺调控肺癌小鼠Bcl-2、Bax蛋白的表达*[J]. 中国肿瘤临床, 2010, 37(19): 1086-1088. DOI: 10.3969/j.issn.1000-8179.2010.19.002
引用本文: 谭明旗, 孙惠梅, 边明艳. HA14-1 联合环磷酰胺调控肺癌小鼠Bcl-2、Bax蛋白的表达*[J]. 中国肿瘤临床, 2010, 37(19): 1086-1088. DOI: 10.3969/j.issn.1000-8179.2010.19.002
TAN Mingqi, SUN Huimei, BIAN Mingyan. HA14-1 Combined with Cyclophosphamide Modulates the Expression of Bcl-2 and Bax in Lung Cancer in Mice[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2010, 37(19): 1086-1088. DOI: 10.3969/j.issn.1000-8179.2010.19.002
Citation: TAN Mingqi, SUN Huimei, BIAN Mingyan. HA14-1 Combined with Cyclophosphamide Modulates the Expression of Bcl-2 and Bax in Lung Cancer in Mice[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2010, 37(19): 1086-1088. DOI: 10.3969/j.issn.1000-8179.2010.19.002

HA14-1 联合环磷酰胺调控肺癌小鼠Bcl-2、Bax蛋白的表达*

HA14-1 Combined with Cyclophosphamide Modulates the Expression of Bcl-2 and Bax in Lung Cancer in Mice

  • 摘要: 目的:探讨HA14-1 联合环磷酰胺对肺癌小鼠Bcl- 2、Bax 蛋白的表达。方法:建立小鼠肿瘤模型,分为生理盐水组、HA14-1 组、环磷酰胺组和HA14-1 + 环磷酰胺组,应用Western blot和免疫组化方法检测Bcl- 2、Bax 的蛋白表达。结果:HA14-1组、环磷酰胺组、HA14-1 + 环磷酰胺组较生理盐水组Bcl- 2 表达减少、Bax 表达增加(P<0.05),HA14-1 + 环磷酰胺组较单一的HA14-1 组或环磷酰胺组Bcl- 2 表达明显减少、Bax 表达明显增加(P<0.05)。 结论:HA14-1 可以通过抑制Bcl- 2 的表达,增加Bax的表达,从而促进肿瘤细胞的凋亡,同时增强环磷酰胺的抗肿瘤特性。

     

    Abstract: Objective: To explore the effect of HA14-1 combined with cyclophosphamide (CTX) on the expression of Bcl- 2 and Bax proteins in lung cancer in mice. Methods: Mouse models of lung carcinoma were established and divided in-to 4 groups: the HA 14-1 group, the CTX group, the combination HA14-1 +CTX group and the normal saline group used as the control. Western blot and immunohistochemistry were applied to detect the expression of Bcl-2 and Bax.Results: The HA14-1 group, the CTX group and the HA14-1 +CTX group had lower Bcl-2 protein expression and higher Bax expression compared with the control group (P<0.05). The HA 14-1 +CTX group had the lowest Bcl-2 protein expression and the high-est Bax protein expression ( P<0.05). Conclusion:HA14-1 can promote tumor cell apoptosis and enhance the efficacy of CTX chemotherapy by downregulating Bcl-2 expression and upregulating Bax expression.

     

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