盘点:前列腺癌相关分子机制进展(六)

2021-04-30 AlexYang MedSci原创

【1】Prostate:Vinculin通过调节肿瘤细胞的入侵、迁移和增殖来协调前列腺癌的进展

【1】Prostate:Vinculin通过调节肿瘤细胞的入侵、迁移和增殖来协调前列腺癌的进展

前列腺癌(PCa)是导致男性死亡的主要原因,仍旧需要进一步开发有效治疗PCa的治疗方法。

最近,有研究人员调查了vinculin(VCL)在PCa体外和体内进展中的潜在作用。

研究人员基于TCGA数据库调查了VCL启动子的甲基化水平。通过qRT-PCR、Western blot分析和免疫荧光证实了VCL基因表达的敲除效果。此外,研究人员还使用了鬼笔环肽染色法检测了PCa细胞的形态学变化;还将肿瘤细胞注射到BALB/c裸鼠右侧产生的皮下异种移植模型,调查了VCL在体内肿瘤生长中的作用。结果表明,PCa中VCL启动子的甲基化水平随着年龄和结节转移的进展而显著下调。shRNA能够明显降低VCL的表达。重要的是,VCL的敲除显著改变了细胞形态;抑制了PCa细胞的迁移、侵袭和移动,并抑制了PCa细胞在体外克隆形成和生存能力。此外,VCL的下调能够抑制体内肿瘤的生长。

最后,研究人员指出,他们的研究全面评估了VCL在体内和体外PCa进展中的作用。研究结果表明了VCL可以成为PCa预后和治疗的潜在靶点。

【2】Oncogene:核βArrestin1能够调控去势抵抗性前列腺癌的雄激素受体功能

前列腺癌(PC)向终末期去势抗性PC(CRPC)的进展涉及一系列不同的中间产物,雄激素受体(AR)是PC启动和进展为CRPC的关键组分。因此,鉴定参与AR表达和功能调控的因子是改善疾病结果必要的第一步。

最近,有研究人员确定了广泛表达的βArrestin 1(βArr1)可作为CRPC中AR功能的调节因子。

研究人员对公共数据集的无偏基因表达分析显示,与正常组织相比,CRPC中ARRB1(编码βArr1的基因)的水平增加。βArr1的表达与这些数据集中AR转录功能的增强有关。βArr1同时分布到细胞核和细胞质,机理研究表明,核中的而非细胞质中的βArr1与AR和AR共调控因子βCatenin形成复合物,并且异源三聚体蛋白复合物被招募到AR调控基因的雄激素响应元件上。在功能上,研究人员证明了βArr1的缺失能够减弱PC细胞和肿瘤的生长和转移,并且恢复细胞核的表达,但不能恢复细胞质的表达,βArr1可以恢复小鼠体外的PC克隆生长和Matrigel的侵袭以及肿瘤的生长和转移。

最后,研究人员指出,靶向βArr1调控的AR转录功能,也许可用于开发治疗致死性CRPC的新药。

【3】Cancer:BRCA1/2-、CDK12-和ATM-突变的转移去势抵抗性前列腺癌的差异化治疗结果

DNA损伤修复突变(DDRm)在转移去势抵抗性前列腺癌(mCRPC)患者中很常见。对该类人群的最佳标准治疗还没有很好的阐述。

最近,有研究人员对mCRPC和DDRm患者进行了一项多机构、回顾性研究。

研究人员收集了患者数据,包括系统治疗和响应。在149名mCRPC男性患者中观察到的最常见的DDRm是BRCA1/2(44%)、CDK12(32%)和ATM(15%)。大多数人接受一线阿比特龙(40%)或恩杂鲁胺(30%)治疗。一线阿比特龙治疗的PSA50率在CDK12(52%)中低于BRCA1/2(89%;P=0.02)。一线阿比特龙或恩杂鲁胺治疗后,与阿比特龙或恩杂鲁胺(33个月)、多西他赛(17个月)或卡巴他赛(11个月)相比,二线卡铂化疗的OS中位数最长(38个月;P=0.02)。BRCA1/2(79%)对基于卡铂的化疗的PSA50反应高于ATM(14%;P=0.02)或CDK12(38%;P=0.08)。在多变量分析中,特异性DDRm类型和一线治疗均与OS改善无关。

最后,研究人员指出,BRCA1/2突变的患者对标准疗法的反应一般较好,而ATM或CDK12突变的患者则较差。DDRm类型并不能独立预测OS。在一线阿比特龙或恩杂鲁胺进展后,基于卡铂的化疗与最长的OS相关。他们的发现可为治疗讨论和临床试验设计提供信息,且仍需要前瞻性验证。

【4】Prostate Cancer P D:CASC11能够促进前列腺癌细胞的侵袭性

前列腺癌是发达国家男性中继肺癌之后最常见的恶性肿瘤。迫切需要对PCa潜在的分子机制进行研究来开发更好的治疗策略和更有效的治疗靶点。

最近,有研究人员调查了CASC11与miR-145和IGF1R在PCa细胞恶性进展过程中可能的功能。

研究人员首先调查了CASC基因家族非编码成员的致癌可能,分析了CASC11过表达对DU145、LNCaP和PC3 PCa细胞增殖、迁移和克隆形成能力的影响。之后,他们在体外模型中探索了CASC11、miR-145和IGF1R表达的关联及其对PI3K/AKT/mTOR信号通路的影响。芯片分析显示,在CASC家族中,考虑到其差异性表达以及与患者总生存的关联,只有CASC11表现出一致的结果。研究人员阐释了CASC11的异位过表达显著增加了所有三个细胞系的增殖、克隆形成和迁移能力。CASC11过表达能够引起miR-145的抑制和IGF1R的过表达,导致PI3K/AKT/mTOR信号通路的激活。

最后,研究人员指出,与相应的对照组相比,CASC11在PCa细胞和临床肿瘤样本中上调,揭示了异位CASC11过表达通过CASC11/miR-145/IGF1R信号途径促进与PCa进展相关的细胞学表型。

【5】Cell Death Dis:FGF21能够促进前列腺癌细胞的自噬

成纤维细胞生长因子21(FGF21)在调节葡萄糖和脂质代谢中起着重要作用,但其在癌症中的作用研究较少。

最近,有研究人员调查了FGF21在前列腺癌(PCa)发展中的作用。

研究人员发现,FGF21的表达在PCa组织和细胞系中明显下调。FGF21能够抑制LNCaP细胞(一种PCa细胞系)的增殖和克隆的形成,并促进细胞凋亡。FGF21还能抑制PCa细胞的迁移和侵袭。GO分析和KEGG分析显示,FGF21与自噬和磷脂酰肌醇3-激酶-Akt激酶-哺乳动物雷帕霉素靶点(PI3K-Akt-mTOR)途径有关。从机制上讲,FGF21通过抑制PI3K-Akt-mTOR-70S6K通路促进LNCaP细胞的自噬。此外,FGF21还能够抑制裸鼠体内PCa肿瘤的发生。

最后,研究人员指出,他们的结果表明了FGF21能够抑制PCa细胞增殖,并通过促进自噬作用促进PCa细胞凋亡。因此,FGF21可能是PCa治疗中的一个潜在的新靶点。

 

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    2021-07-23 六神草

    学习了

    0

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    2021-07-11 ms2091037772680667

    学习了

    0

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    2021-05-03 suncunfu

    学习了

    0

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    2021-05-02 njwbhuang

    很好的文献,学习了

    0

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    2021-05-01 15942a55d4m

    vinculin(VCL)在PCa体外和体内进展中的潜在作用!

    0

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    2021-05-01 肿肿

    机制研究离临床仍然有距离,不过与临床结合思考,仍然有帮助的,不能仅仅是纯临床思维,转化思维同样重要

    0

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    2021-05-01 misszhang

    前列腺癌相关研究,学习了,谢谢梅斯

    0

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