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首页> 外文期刊>Molecular cancer research: MCR >Cyclooxygenase-2 Inhibitor Induces Apoptosis in Breast Cancer Cells in an In vivo Model of Spontaneous Metastatic Breast Cancer.
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Cyclooxygenase-2 Inhibitor Induces Apoptosis in Breast Cancer Cells in an In vivo Model of Spontaneous Metastatic Breast Cancer.

机译：在自发转移性乳腺癌的体内模型中，环氧合酶2抑制剂诱导乳腺癌细胞凋亡。

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Cyclooxygenase-2 (COX-2) inhibitors are rapidly emerging as a new generation of therapeutic drug in combination with chemotherapy or radiation therapy for the treatment of cancer. The mechanisms underlying its antitumor effects are not fully understood and more thorough preclinical trials are needed to determine if COX-2 inhibition represents a useful approach for prevention and/or treatment of breast cancer. The purpose of this study was to evaluate the growth inhibitory mechanism of a highly selective COX-2 inhibitor, celecoxib, in an in vivo oncogenic mouse model of spontaneous breast cancer that resembles human disease. The oncogenic mice carry the polyoma middle T antigen driven by the mouse mammary tumor virus promoter and develop primary adenocarcinomas of the breast. Results show that oral administration of celecoxib caused significant reduction in mammary tumor burden associated with increased tumor cell apoptosis and decreased proliferation in vivo. In vivo apoptosis correlated with significant decrease in activation of protein kinase B/Akt, a cell survival signaling kinase, with increased expression of the proapoptotic protein Bax and decreased expression of the antiapoptotic protein Bcl-2. In addition, celecoxib treatment reduced levels of proangiogenic factor (vascular endothelial growth factor), suggesting a role of celecoxib in suppression of angiogenesis in this model. Results from these preclinical studies will form the basis for assessing the feasibility of celecoxib therapy alone or in combination with conventional therapies for treatment and/or prevention of breast cancer.
机译：环氧合酶-2（COX-2）抑制剂是与化疗或放疗结合用于治疗癌症的新一代治疗药物，正在迅速兴起。其抗肿瘤作用的机制尚不完全清楚，需要更彻底的临床前试验来确定抑制COX-2是否代表一种预防和/或治疗乳腺癌的有用方法。这项研究的目的是评估在类似于人类疾病的自发性乳腺癌的体内致癌小鼠模型中，高选择性COX-2抑制剂塞来昔布的生长抑制机制。致癌小鼠携带由小鼠乳腺肿瘤病毒启动子驱动的多瘤中期T抗原，并发展为乳腺原发性腺癌。结果表明，塞来昔布口服给药可显着减少乳腺肿瘤负担，从而增加肿瘤细胞凋亡并降低体内增殖。体内凋亡与蛋白激酶B / Akt（一种细胞存活信号激酶）的活化显着降低有关，与促凋亡蛋白Bax的表达增加和抗凋亡蛋白Bcl-2的表达减少有关。另外，塞来昔布治疗降低了促血管生成因子（血管内皮生长因子）的水平，表明塞来昔布在该模型中在抑制血管生成中具有作用。这些临床前研究的结果将成为评估塞来昔布单独治疗或与常规疗法联合治疗和/或预防乳腺癌的可行性的基础。

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