Evidence map›Paper›PMID 31791014›Full record

ArticleMolecular therapy. Nucleic acids2019

Role of linc00174/miR-138-5p (miR-150-5p)/FOSL2 Feedback Loop on Regulating the Blood-Tumor Barrier Permeability.

Jizhe Guo, Shuyuan Shen, Xiaobai Liu, Xuelei Ruan, Jian Zheng, Yunhui Liu, Libo Liu, Jun Ma, Teng Ma, Lianqi Shao and 3 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Jizhe GuoDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Shuyuan ShenDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Xiaobai LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China.
Xuelei RuanDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Jian ZhengDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China.
Yunhui LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China.
Libo LiuDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Jun MaDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Teng MaDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Lianqi ShaoDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China.
Di WangDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China.
Chunqing YangDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, People's Republic of China; Liaoning Research Center for Translational Medicine in Nervous System Disease, Shenyang 110004, People's Republic of China; Key Laboratory of Neuro-oncology in Liaoning Province, Shenyang 110004, People's Republic of China.
Yixue XueDepartment of Neurobiology, School of Life Sciences, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110122, People's Republic of China; Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122, People's Republic of China. Electronic address: xueyixue888@163.com.
China Medical University · CNShenyang Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-tumor barrier (BTB) limits the transport of chemotherapeutic drugs to brain tumor tissues and impacts the treatment of glioma. Long non-coding RNAs play critical roles in various biological processes of tumors; however, the function of these in BTB permeability is still unclear. In this study, we have identified that long intergenic non-protein coding RNA 174 (linc00174) was upregulated in glioma endothelial cells (GECs) from glioma tissues. Additionally, linc00174 was also upregulated in GECs from the BTB model in vitro. Knock down of linc00174 increased BTB permeability and reduced the expression of the tight junction-related proteins ZO-1, occludin, and claudin-5. Both bioinformatics data and results of luciferase reporter assays demonstrated that linc00174 regulated BTB permeability by binding to miR-138-5p and miR-150-5p. Furthermore, knock down of linc00174 inhibited FOSL2 expression via upregulating miR-138-5p and miR-150-5p. FOSL2 interacted with the promoter regions and upregulated the promoter activity of ZO-1, occludin, claudin-5, and linc00174 in GECs. In conclusion, the present study demonstrated that the linc00174/miR-138-5p (miR-150-5p)/FOSL2 feedback loop played an essential role in regulating BTB permeability.

Indexed as

blood-tumor barrierFOSL2linc00174miR-138-5pmiR-150-5p

Identifiers

PMID31791014
PMCPMC6906710
OpenAlexW2990631592

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.