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PLoS Biol:中美学者揭示TRIM59调控乳腺癌增殖与转移的新机制

2018-11-18 佚名 生物通

浙江大学医学院附属邵逸夫医院韩卫东课题组及美国德州农工大学Yubin Zhou课题组揭示了TRIM59蛋白促进乳腺癌增殖与转移的新机制。

浙江大学医学院附属邵逸夫医院韩卫东课题组及美国德州农工大学Yubin Zhou课题组揭示了TRIM59蛋白促进乳腺癌增殖与转移的新机制。


图1. TRIM59通过抑制p62介导的PDCD10的选择性自噬降解从而促进乳腺癌增殖与转移

研究成果以“TRIM59 promotes breast cancer motility by suppressing p62-selective autophagic degradation of PDCD10”(TRIM59通过抑制p62介导的PDCD10的选择性自噬降解从而促进乳腺癌增殖与转移)为题,于2018年11月8日在PLOS BIOLOGY上在线发表。韩卫东、Yubin Zhou及德州大学健康中心的Leng Han教授为文章的共同通讯作者,谭鹏博士为第一作者。

根据世界卫生组织估计,2018年死于肿瘤的人数达到960万,约占总死亡原因的六分之一。而肿瘤的侵袭与转移是导致肿瘤患者死亡的主要原因。肿瘤细胞通过改变自身形态,在体内采取多种转移模式而迁移并侵袭其他器官以获得自身生存所需的营养。所以一旦肿瘤细胞发生转移,它们就很难被控制和治愈。

近年来,细胞自噬与肿瘤关系的研究越来越多。细胞自噬是一个被精细调控的过程,它既能够通过吞噬清除致突变的有害物质来抑制肿瘤发生,又可以通过向肿瘤细胞提供营养与能量而促进肿瘤的发展。然而,自噬影响肿瘤转移的机制尚未完全明确。TRIM(The tripartite motif)家族蛋白大多都拥有E3泛素化连接酶活性,可通过调节p53和AMPK信号通路及原癌基因的转录激活,在肿瘤细胞代谢和生长凋亡方面发挥重要作用,但是TRIM蛋白与肿瘤细胞运动及肿瘤转移方面的研究却仍是空白。

该研究通过对TCGA(the Cancer Genome Atlas)数据库和乳腺癌患者临床样本的分析发现:TRIM59蛋白在转移性乳腺癌中表达异常升高,并且其表达量与病人生存时间呈负相关。在乳腺癌细胞中敲降或敲除TRIM59可增加细胞凋亡并抑制细胞增殖和迁移,而过表达则出现相反的结果。

研究组进一步通过定量蛋白组学分析发现,TRIM59调控乳腺癌细胞生长并不是通过常见的MAPK和p53信号通路,而是与c-Myc、IGF1R、VEGFR2和INPP4b通路有关。

另一方面,TRIM59促进乳腺癌转移的机制则是通过抑制MLC和ERM的磷酸化,从而促进肌动球蛋白的伸缩性和细胞变形迁移、减少细胞粘附分子如E-cadherin的表达,以及增加细胞内β-catenin的水平来激活转移相关的Wnt信号通路来实现的。

为了找到TRIM59的直接作用靶点,该课题组进行了酵母双杂交实验,并将PDCD10锁定为重要的候选分子。通过进一步探索证实TRIM59可以通过RING结构域直接与PDCD10相互作用,阻断RNFT1介导的K63泛素化从而抑制p62介导的PDCD10的自噬性降解,影响PDCD10控制的ROCK信号通路,进而促进细胞形态变化和肿瘤细胞生长转移。

该研究揭示了TRIM59通过抑制PDCD10的自噬性降解来促进乳腺癌生长转移的新机制,提示阻断TRIM59和PDCD10之间的相互作用可作为治疗乳腺癌的潜在新策略。该研究是在国家自然科学基金(项目编号:81572592, 81572361)的资助下完成的。

原始出处:Tan P, Ye Y, He L, er al. TRIM59 promotes breast cancer motility by suppressing p62-selective autophagic degradation of PDCD10. PLoS Biol. 2018 Nov 8;16(11):e3000051. 

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    2019-02-15 sunylz
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    2018-11-21 杨帆7792

    学习 学习 谢谢

    0

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    2018-11-19 lietome2

    好文,值得点赞!认真学习了,把经验应用于实践,为患者解除病痛。

    0

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    2018-11-18 医者仁心5538

    学习了

    0

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近日,一项大型研究结果显示:早起的女性可能会降低患乳腺癌的风险。

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