Cell Death & Disease:膀胱癌中氧化亚铜纳米粒子能够激活活性氧诱导的细胞凋亡

2020-05-31 AlexYang MedSci原创

顺铂化疗是晚期膀胱癌的一线治疗方法。然而,超过50%的患者不适合进行顺铂化疗,因此开发新的治疗药物非常迫切。氧化亚铜纳米粒子(CONPs)是一种新的纳米治疗药物,在许多类型的癌症治疗中均证实是有效的。

顺铂化疗是晚期膀胱癌的一线治疗方法。然而,超过50%的患者不适合进行顺铂化疗,因此开发新的治疗药物非常迫切。氧化亚铜纳米粒子(CONPs)是一种新的纳米治疗药物,在许多类型的癌症治疗中均证实是有效的。

最近,有研究人员发现,CONPs对不同的膀胱癌细胞系(T24、J82、5637和UMUC3)具有剂量依赖和时间依赖的抑制作用,且对非癌上皮细胞(SVHUCs)具有轻度的抑制作用。CONPs能够引起膀胱癌细胞中的细胞周期阻滞和细胞凋亡。研究人员进一步阐释了CONP诱导的细胞毒性机制为细胞凋亡,通过活性氧激活ERK信号途径和自噬引起。更多的是,CONPs对膀胱癌的细胞毒性影响在原位异种移植和皮下裸鼠模型中均得到了证实,表明了CONPs能够显著的抑制体内膀胱癌的生长。进一步的药物组合试验表明,CONPs与顺铂和吉西他滨在体外具有协同作用。研究人员还进一步证明了CONPs能够增强吉西他滨体内抗肿瘤活性且不加重副作用,表明了CONPs与吉西他滨可以组合用于膀胱内化疗。

最后,研究人员指出,他们的预临床数据表面CONPs是很有前景的膀胱癌纳米药物,并且为CONPs和吉西他滨组合在膀胱内膀胱癌治疗提供了新的认识。

原始出处:

Qiao Xiong, Anwei Liu, Qian Ren et al. Cuprous oxide nanoparticles trigger reactive oxygen species-induced apoptosis through activation of erk-dependent autophagy in bladder cancer. Cell Death & Disease. 14 May 2020

 

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    2021-04-11 维他命
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    2020-06-02 徐岩
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    2020-06-02 cy0328
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    2020-05-31 留走人康

    膀胱癌真怪,明明是免疫敏感性肿瘤,为什么PD-1治疗效果不好呢?难道靶点不对?将来CD47会不会有效

    0

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年龄相关的听力损失(ARHL)是听觉系统老化的结果。ARHL中细胞死亡最清楚的机制为由于活性氧种类产生的增加导致的细胞凋亡。据此,有研究人员假设由于褪黑素具有高度的抗氧化能力和在线粒体中的作用,认为能够预防或者延迟外毛细胞的功能异常(HCD)。最近,有研究人员在一个易感的小鼠C57BL/6J模型中评估了ARHL过程中,褪黑素对HCD功能异常的预防作用情况。研究人员将C57BL/6J动物分成2个组:

NATURE:凋亡细胞释放代谢物作为“再见”信号

凋亡细胞不是等待清除的惰性细胞,而是释放代谢物作为“再见”信号,积极调节组织的结果。

Cell Death Dis:lncR-TUG1/miR-9/KLF5通路调控心肌细胞凋亡

非编码RNA参与多种心脏生理病理过程,包括心肌梗死(MI)。近日,研究人员发现长链非编码RNA lncR-TUG1(牛磺酸上调基因1)、miR-9a-5p(miR-9)和KLF5(Krüppel样因子5)之间存在相互作用。在缺血性心脏和体外培养的暴露于H2O2的心肌细胞中,LncR-TUG1表达水平上调。而敲低lncR-TUG1可以显著改善MI小鼠的受损心脏功能。进一步研究表明,lncR-TUG1

Cell Death & Differentiation:去泛素化酶USP33能够抑制多烯紫杉醇诱导的细胞凋亡

去势抵抗性前列腺癌的治疗(CRPC)仍旧面临许多挑战。多烯紫杉醇是CRPC患者中常用的一种化疗药物。然而,基于多烯紫杉醇的化疗常常会引起多烯紫杉醇抗性,部分是CRPC细胞对多烯紫杉醇诱导的细胞凋亡抗性。最近,有研究人员报道了去泛素化酶USP33能够抑制多烯紫杉醇诱导的前列腺癌细胞死亡,包括了不依赖雄激素的前列腺癌细胞。USP33在前列腺癌细胞和组织中过表达。USP33表达的抑制或者敲除能够增强多烯