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长链非编码RNA UCA1通过靶向iASPP与miR-182相互作用,调节胶质瘤的增殖和迁移。

The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP.

作者信息

He Zongze, Wang Yujue, Huang Guangfu, Wang Qi, Zhao Dongdong, Chen Longyi

机构信息

Department of Neurosurgery, Hospital of University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, Chengdu, Sichuan Province 610072, China.

Department of Neurosurgery, Kai Luan General Hospital, Tangshan City, Hebei Province 063000, China.

出版信息

Arch Biochem Biophys. 2017 Jun 1;623-624:1-8. doi: 10.1016/j.abb.2017.01.013. Epub 2017 Jan 28.

DOI:10.1016/j.abb.2017.01.013
PMID:28137422
Abstract

Long non-coding RNA (lncRNA) urothelial carcinoma associated 1 (UCA1) has been reported to be involved in the development and progression of many types of tumors including breast cancer, gastric cancer, and bladder cancer. However, the exact effects and molecular mechanisms of UCA1 in glioma progression remain unclear up to now. In this study, we firstly found that UCA1 was upregulated in glioma tumor samples and negatively correlated with survival time. Then, we investigated the role of UCA1 in human glioma cell lines. Our results showed that upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation. Taken together, UCA1 might promote proliferation and migration of glioma, to regulate the tumor growth and metastasis via miR-182 dependent iASPP regulation. Therefore, lncRNA-UCA1 could be regarded as a therapeutic target in human glioma.

摘要

据报道,长链非编码RNA(lncRNA)尿路上皮癌相关因子1(UCA1)参与了包括乳腺癌、胃癌和膀胱癌在内的多种肿瘤的发生和发展。然而,截至目前,UCA1在胶质瘤进展中的具体作用和分子机制仍不清楚。在本研究中,我们首先发现UCA1在胶质瘤肿瘤样本中上调,且与生存时间呈负相关。然后,我们研究了UCA1在人胶质瘤细胞系中的作用。我们的结果表明,lncRNA-UCA1在胶质瘤组织和细胞系中的上调可通过与miR-182相互作用促进胶质瘤细胞增殖和迁移,而敲低UCA1可抑制人胶质瘤细胞的增殖和迁移。此外,UCA1诱导的胶质瘤细胞增殖调控需要miR-182依赖的p53凋亡刺激蛋白抑制剂(iASPP)。综上所述,UCA1可能通过miR-182依赖的iASPP调控促进胶质瘤的增殖和迁移,从而调节肿瘤的生长和转移。因此,lncRNA-UCA1可被视为人类胶质瘤的治疗靶点。

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