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Oncogene:对环氧酶2调控的蛋白裂解酶激活的抑制能抑制前列腺癌细胞死亡和转移

2017-04-30 AlexYang MedSci原创

慢性炎症在癌症的发生和发展中具有重要作用。环氧合酶-2(COX-2)在产生前列腺素并引起炎症中是一个关键的酶,COX-2在前列腺癌(PCa)中经常超表达并且和PCa细胞的侵入和转移相关。最近,有研究人员就COX-2促进PCa细胞侵入和转移的分子机制和COX-2抑制剂在选择的PCa发展模型中的效应进行了研究。研究结果表明,在高度侵入性PCa细胞中,COX-2和白介素1β(IL-1β)的表达上调,并且

慢性炎症在癌症的发生和发展中具有重要作用。环氧合酶-2(COX-2)在产生前列腺素并引起炎症中是一个关键的酶,COX-2在前列腺癌(PCa)中经常超表达并且和PCa细胞的侵入和转移相关。

最近,有研究人员就COX-2促进PCa细胞侵入和转移的分子机制和COX-2抑制剂在选择的PCa发展模型中的效应进行了研究。研究结果表明,在高度侵入性PCa细胞中,COX-2和白介素1β(IL-1β)的表达上调,并且与膜锚定的丝氨酸蛋白裂解酶的激活水平相关。在PCa样品中,COX-2的表达水平增加并且与蛋白裂解酶的水平相关。更多的是,COX-2的超表达或者COX-2的产物前列腺素E2(PGE2)可以引起蛋白裂解酶活性的增加和PCa细胞的侵入,而COX-2的沉默可起到相反的作用。另外,在原位异种种植模型中,西乐葆和硫化舒林酸产生的环氧酶2调控的蛋白裂解酶激活的抑制可以抑制不依赖雄激素和COX-2超表达的PCa PC-2细胞侵入、肿瘤生长和肺转移。最后,研究人员指出,COX-2/蛋白裂解酶信号可以导致侵入、肿瘤生长和COX-2超表达和不依赖雄激素PCa细胞转移。

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    2017-09-14 cy0324
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    2017-05-02 yxch36
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    2017-05-02 zsyan
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铂化合物的化学抵抗性是导致晚期膀胱癌(BC)治疗失败的致死的主要原因。但是,潜在的机制仍旧不清楚,这也阻碍了治疗策略的发展。最近的研究数据表明丙酮酸激酶M2(PKM2),一个瓦博格效应糖解酶,在BC中的表达水平强烈地提高了。最近,有研究人员就PKM2在化学抵抗性中的角色和是否抑制PKM2就可以增加对铂化合物的抵抗性和减少BC生长和发展进行了研究。研究发现,紫草素结合PKM2并能抑制BC细胞存活,且

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