Gut:浙江大学医学院徐骁教授团队Gut发表肝癌干性研究新成果

2019-12-07 佚名细胞

<div>近日，国际著名<a class="channel_keylink" href="http://ipsen2017.medsci.cn/ipsen/sporty/show-details/3074/2" target="_blank"><a class="channel_keylink" href="http://ipsen2017.medsci.cn/ipsen/sporty/show-details/69/2" target="_blank">消化</a></a>杂志Gut在线发表了浙江大学医学院徐骁教授团队的题为USP22 promotes hypoxia-induced hepatocellular carcinoma stemness by a HIF1α/USP22 positive feedback loop upon TP53 inactivation的研究论文。</div><div><br>肿瘤组织中某些细胞亚群的<a class="channel_keylink" href="//m.capotfarm.com/article/list.do?q=%E

近日，国际著名消化杂志Gut在线发表了浙江大学医学院徐骁教授团队的题为USP22 promotes hypoxia-induced hepatocellular carcinoma stemness by a HIF1α/USP22 positive feedback loop upon TP53 inactivation的研究论文。

肿瘤组织中某些细胞亚群的干细胞特性被认为与肿瘤的发生、侵袭转移、血管新生和放化疗抵抗密切相关，靶向肿瘤干细胞特性已成为克服肿瘤细胞耐药、抑制肿瘤转移与复发的重要策略。该研究发现，去泛素化蛋白酶 ubiquitin-specific protease 22(USP22) 可在缺氧条件下稳定肝癌细胞中的HIF1α蛋白；而在TP53失活的肝癌细胞中，HIF1α可促进USP22的转录表达。USP22与HIF1α组成的正反馈调节通路可促进肝癌细胞的干性表型。分析肝癌病人的组织标本发现，TP53失活突变合并USP22和HIF1α高表达的患者预后更差。TP53失活突变是肝癌发生发展中的常见事件，与肝癌的恶性生物学行为密切相关。该研究解析了USP22/HIF1α调控环路在TP53失活突变肝癌中的关键作用，揭示了维持肝癌干性的全新分子通路。

另外，鉴于目前缺少USP22的特异性抑制剂，该团队开发了一种新型肿瘤内活性氧响应的纳米基因药物，特异性降低肿瘤内USP22的表达，可显着抑制肝癌肿瘤的生长，并且增强肝癌细胞对索拉菲尼的敏感性，为肝癌的精准靶向治疗提供了有效的策略。

该论文通讯作者为***、浙江大学医学院附属第一医院肝胆胰外科徐骁教授。浙江大学医学院附属第一医院肝胆胰外科医师凌孙彬博士、博士生单巧楠、硕士生詹启帆为论文第一作者。该项研究受教育部***奖励计划、国家科技重大专项及国家杰出青年科学基金等项目资助，得到浙大一院领导和相关科室的支持。郑树森院士、申有青教授及美国宾夕法尼亚大学医学院部分学者给予大力支持。

原始出处：

Sunbin Ling #, Qiaonan Shan #, Xiao Xu ,et al.USP22 Promotes Hypoxia-Induced Hepatocellular Carcinoma Stemness by a HIF1a/USP22 Positive Feedback Loop Upon TP53 Inactivation .Gut.2019 Nov 27,PMID: 31776228 DOI: 10.1136/gutjnl-2019-319616

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2020-05-27 朱睿睿

#医学院#

78 0
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2020-08-05 一闲

#浙江大学#

93 0
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2019-12-12 wgx306

#新成果#

74 0
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2019-12-07 留走人康

肝癌，接下来就要细分了，对于体质好的病人，能否将PD-1类+抗血管新生+放疗等相结合，甚至有必要用TACE进行减负

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