撤稿文章：长链非编码RNA PTPRG-AS1通过吸附miR-185-5p调控胶质瘤细胞生长。
Retracted Article: Long noncoding RNA PTPRG-AS1 regulates growth of glioma cells by sponging miR-185-5p.
作者信息
Xu Chenyang, Li Zhenjiang, He Tao, Yuan Bingjian, Ding Bingqian
机构信息
Department of Neurosurgery, Huaihe Hospital of Henan University No. 1, North Baogong Rd, Gulou Kaifeng Henan 475000 China
出版信息
RSC Adv. 2019 Apr 8;9(19):10870-10880. doi: 10.1039/c8ra09546a. eCollection 2019 Apr 3.
Previous studies have found that long noncoding RNA (lncRNA) protein tyrosine phosphatase, receptor type, G, antisense (PTPRG-AS1) was upregulated in glioma cells. Our study aimed to explore the detailed molecular mechanisms of PTPRG-AS1 involved in glioma progression. qRT-PCR assay was performed to measure the expressions of PTPRG-AS1 and microRNA-185-5p (miR-185-5p). Cell viability, migration, invasion, and apoptosis were determined by CCK-8 assay, colony formation assay, transwell assay, and flow cytometry assay. Autophagy was evaluated using GFP-LC3 puncta analysis and western blot. Luciferase reporter and RIP assays were employed to explore the association between PTPRG-AS1 and miR-185-5p. Our data showed PTPRG-AS1 was upregulated in glioma cells and tissues. Besides, high expression of PTPRG-AS1 was positively associated with a low survival rate. Upregulation of PTPRG-AS1 promoted proliferation, migration, invasion, colony formations, and autophagy, and inhibited cell apoptosis in U373-MG cells. By contrast, PTPRG-AS1 downregulation had the inverse effect in SHG44 cells. PTPRG-AS1 negatively regulated the expression of miR-185-5p in U373-MG and SHG44 cells and the expression of miR-185-5p was decreased in glioma tissues and cells. In addition, miR-185-5p overexpression suppressed proliferation, metastasis, colony formations, and autophagy, while inducing cell apoptosis in SHG44 cells. As expected, miR-185-5p depletion exhibited the inverse effect in U373-MG cells. Enhanced expression of miR-185-5p attenuated the effect of PTPRG-AS1 upregulation on U373-MG cells, while silencing of miR-185-5p undermined the effect of downregulation of PTPRG-AS1 on SHG44 cells. Our data disclosed that LncRNA PTPRG-AS1 was upregulated in glioma cells and tissues. PTPRG-AS1 regulated glioma proliferation, invasion, migration, apoptosis and autophagy by sponging miR-185-5p . A new signaling pathway PTPRG-AS1/miR-185-5p was first observed in glioma.
先前的研究发现，长链非编码RNA（lncRNA）蛋白酪氨酸磷酸酶受体型G反义链（PTPRG-AS1）在胶质瘤细胞中表达上调。我们的研究旨在探索PTPRG-AS1参与胶质瘤进展的详细分子机制。采用qRT-PCR检测法检测PTPRG-AS1和微小RNA-185-5p（miR-185-5p）的表达。通过CCK-8检测法、集落形成检测法、Transwell检测法和流式细胞术检测法测定细胞活力、迁移、侵袭和凋亡情况。使用绿色荧光蛋白标记的微管相关蛋白1轻链3（GFP-LC3）斑点分析和蛋白质免疫印迹法评估自噬。采用荧光素酶报告基因检测和RNA免疫沉淀（RIP）检测来探究PTPRG-AS1与miR-185-5p之间的关系。我们的数据表明，PTPRG-AS1在胶质瘤细胞和组织中表达上调。此外，PTPRG-AS1的高表达与低生存率呈正相关。PTPRG-AS1的上调促进了U373-MG细胞的增殖、迁移、侵袭、集落形成和自噬，并抑制了细胞凋亡。相比之下，PTPRG-AS1的下调在SHG44细胞中产生相反的作用。PTPRG-AS1在U373-MG和SHG44细胞中负向调节miR-185-5p的表达，且miR-185-5p在胶质瘤组织和细胞中的表达降低。此外，miR-185-5p的过表达抑制了SHG44细胞的增殖、转移、集落形成和自噬，同时诱导细胞凋亡。正如预期的那样，miR-185-5p的缺失在U373-MG细胞中产生相反的作用。miR-185-5p表达的增强减弱了PTPRG-AS1上调对U373-MG细胞的影响，而miR-185-5p的沉默则削弱了PTPRG-AS1下调对SHG44细胞的影响。我们的数据表明，lncRNA PTPRG-AS1在胶质瘤细胞和组织中表达上调。PTPRG-AS1通过海绵吸附miR-185-5p来调节胶质瘤的增殖、侵袭、迁移、凋亡和自噬。在胶质瘤中首次观察到一条新的信号通路PTPRG-AS1/miR-185-5p。
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