Suppr超能文献

长链非编码RNA MALAT1与miR-204相互作用,通过靶向CXCR4调节人肝门部胆管癌的增殖、迁移和侵袭。

Long Non-Coding RNA MALAT1 Interacts With miR-204 to Modulate Human Hilar Cholangiocarcinoma Proliferation, Migration, and Invasion by Targeting CXCR4.

作者信息

Tan Xinyu, Huang Zhiguo, Li Xiaogang

机构信息

Department of Emergency, Xiangya Hospital, Central South University, Changsha City 410000, China.

出版信息

J Cell Biochem. 2017 Nov;118(11):3643-3653. doi: 10.1002/jcb.25862. Epub 2017 Jul 11.

Abstract

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the development and progression of many types of tumors. An aberrant expression of MALAT1 was observed in many kinds of cancers. However, the exact effects and molecular mechanisms of MALAT1 in human hilar cholangiocarcinoma (HCCA) progression are still unknown. Here, we investigated the role of MALAT1 in human HCCA cell lines and clinical tumor samples in order to determine the function of this lncRNA. In our research, lncRNA-MALAT1 was specifically upregulated in HCCA tissues and cell lines, and was associated with pathological T stage, a larger tumor size, and perineural invasion. Knockdown of MALAT1 inhibited the proliferation, migration, and invasion of human HCCA cell. In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration, and invasion. By using online tools and a series of mechanistic analysis, we also demonstrated that miR-204-dependent CXCR4 regulation was required in MALAT1 modulating HCCA cell growth, migration and invasion. Taken together, our data indicated that MALAT1 might play an oncogenic role in HCCA through miR-204-dependent CXCR4 regulation, and could be regarded as a therapeutic target in HCCA. J. Cell. Biochem. 118: 3643-3653, 2017. © 2017 Wiley Periodicals, Inc.

摘要

转移相关的肺腺癌转录本1(MALAT1)参与多种肿瘤的发生和发展。在多种癌症中均观察到MALAT1的异常表达。然而,MALAT1在人肝门胆管癌(HCCA)进展中的确切作用和分子机制仍不清楚。在此,我们研究了MALAT1在人HCCA细胞系和临床肿瘤样本中的作用,以确定这种长链非编码RNA的功能。在我们的研究中,lncRNA-MALAT1在HCCA组织和细胞系中特异性上调,并且与病理T分期、更大的肿瘤大小和神经周围浸润相关。敲低MALAT1可抑制人HCCA细胞的增殖、迁移和侵袭。此外,趋化因子受体4(CXCR4)参与了MALAT1诱导的人HCCA生长、迁移和侵袭。通过使用在线工具和一系列机制分析,我们还证明在MALAT1调节HCCA细胞生长、迁移和侵袭过程中需要miR-204依赖的CXCR4调控。综上所述,我们的数据表明MALAT1可能通过miR-204依赖的CXCR4调控在HCCA中发挥致癌作用,并可被视为HCCA的一个治疗靶点。《细胞生物化学杂志》118: 3643 - 3653, 2017年。© 2017威利期刊公司

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验