| Yue Li,Yuling Bai,Yan Qi,Chang Cai,Ying Liao,Xiuzhu Liu,Pengcheng He. Expression and role of PTV1 lncRNA in glioma cells progression. Oncol Transl Med, 2021, 7: 51-58. |
| Expression and role of PTV1 lncRNA in glioma cells progression |
| Expression and role of PTV1 lncRNA in glioma cells progression |
| Received:June 07, 2020 Revised:April 23, 2021 |
| DOI：10.1007/s10330-020-0435-5 |
| 中文关键词: |
| 英文关键词: glioma; miRNA-203a; long-chain noncoding RNA; transcription factor PTV1 lncRNA |
| 基金项目:国家自然科学基金面上项目(81472965) |
| Author Name | Affiliation | E-mail | | Yue Li | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | dengdeng9988@163.com | | Yuling Bai | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | | | Yan Qi | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | | | Chang Cai | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | | | Ying Liao | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | | | Xiuzhu Liu | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | | | Pengcheng He* | Department of Neurosurgery, Mianyang Central Hospital, Mianyang 621000, China | yueyue52887@sina.com |
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| 中文摘要: |
| 目的：探讨长链非编码RNA PTV1（LncRNA PTV1）在脑胶质瘤中的表达及通过与miR-203a相互作用介导胶质瘤进展的机制。方法：稳定培养U87、U251细胞，分别转染PTV1 Sh-RNA（SH）或PTV1过表达质粒（OV），检测U87、U251细胞活性的变化。构建胶质瘤移植瘤裸鼠模型，分为U87组、U251组，分别在腋下注射U87-SH、U251-OV细胞，再分别进行miR-203a 激动剂（mimic）、抑制剂(inhibitor)干预，检测小鼠肿瘤内相关蛋白变化。结果：（1）PTV1在胶质瘤组织中的相对表达水平显著高于正常脑组织，在多形性胶质母细胞瘤中的表达水平明显高于低级别胶质瘤。敲低RPTV1后显著抑制了U87细胞的增殖，细胞克隆数较少；过表达RPTV1显著促进了U251细胞的增殖，细胞克隆集落更多（2）双荧光素酶报告显示，SP2是miR-203a的潜在靶基因。在U87细胞中加入miR-203a mimic后，SP2表达水平下降；在U251细胞中加入miR-203a inhibitor后，SP2表达水平显著升高。（3）在U87-SH细胞中过表达SP2的表达，U87-SH细胞的增殖、迁移和侵袭能力得到了明显增强。在U251-OV细胞中下调了SP2的表达，U251-OV细胞的相应活性受到了明显抑制。（4）与对照组相比，U87-SH组小鼠的肿瘤体积明显较小，肿瘤组织中SP2阳性率显著较低，应用miR-203a inhibitor后肿瘤体积又逐渐增大，SP2阳性率又显著升高。与对照组相比，U251-OV组小鼠体积明显较大，肿瘤组织中SP2阳性率显著较高，应用miR-203a mimic后肿瘤体积又明显缩小，SP2阳性率又显著下降。结论：lncRNA PTV1可以作为miR-203a的ceRNA下调SP2表达，促进胶质瘤细胞的增殖和侵袭。LncRNA PTV1可能是一种新的胶质瘤预后生物标志物和治疗靶点。 |
| 英文摘要: |
| Objective The aim of this study was to investigate the expression of PTV1 lncRNA in gliomas and the
mechanism of its interaction with miR-203a.
Methods U87 and U251 cells were cultured stably and transfected with sh-PTV1 or ov-PTV1, respectively.
The proliferative activity of U87 and U251 cells was detected and the transplanted tumor model nude mice
were divided into U87 and U251 groups. U87-sh and u251-ov cells were injected into the armpit, then
miR-203a mic and miR-203a inhibitors were administered to detect the changes in the expression of tumorrelated
proteins.
Results The relative expression of PTV1 in gliomas was significantly higher than that in normal brain
tissues, while in GBM it was significantly higher than that in low-grade gliomas. Knockdown of PTV1
significantly inhibited the proliferation of U87 cells, resulting in fewer cell clones; overexpression of rPTV1
significantly promoted the proliferation of U251 cells, resulting in more cell colonies. The dual Luciferase
Reporter assay showed that SP2 was a potential target of miR-203a. When U87 cells were treated with a
miR-203a mimic, the expression of SP2 decreased; and when U251 cells were treated with a miR-203a
inhibitor, the expression of SP2 increased significantly. SP2 was overexpressed in u87-sh cells and the
proliferation, migration, and invasion of u87-sh cells were significantly enhanced. U251-ov cells showed
the opposite trend. Compared with the control group mice, the tumor volume in u87-sh group mice was
significantly smaller and the positive rate of SP2 in tumor tissue was significantly lower. After administration
of the miR-203a inhibitor, the tumor volume increased gradually and the positive rate of SP2 increased
significantly, while u251-ov mice showed the opposite trend.
Conclusion lncRNA PTV1 can be used as a molecule to interfere with miR-203a expression in order to
downregulate SP2 and to promote the proliferation and invasion of glioma cells. lncRNA PTV1 may be a
new biomarker and therapeutic target for glioma. |
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