Evidence map›Paper›PMID 28969029›Full record

ArticleOncotarget2017

Suppression of CLC-3 chloride channel reduces the aggressiveness of glioma through inhibiting nuclear factor-κB pathway.

Bing Wang, Jing Xie, Hai-Yong He, En-Wen Huang, Qing-Hua Cao, Lun Luo, Yong-Shi Liao, Ying Guo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Therapeutic Promise and Biotechnological Prospects ofInternational journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
  5. Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023
    Review
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  7. Review
  8. Review
  9. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Bing Wang *Department of Neurosurgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Jing Xie *Department of Integrative Oncology, Shanghai Cancer Center, Fudan University, Shanghai, China.
Hai-Yong He *Department of Neurosurgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
En-Wen HuangFaculty of Forensic Medicine, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.
Qing-Hua CaoDepartment of Pathology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Lun LuoDepartment of Neurosurgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Yong-Shi LiaoDepartment of Neurosurgery, The Second Affiliated Hospital, University of South China, Hengyang, China.
Ying GuoDepartment of Neurosurgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CNFudan University Shanghai Cancer Center · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CLC-3 chloride channel plays important roles on cell volume regulation, proliferation and migration in normal and cancer cells. Recent growing evidence supports a critical role of CLC-3 in glioma metastasis, however, the mechanism underlying is unclear. This study finds that CLC-3 is upregulated in glioma tissues and positively correlated with WHO histological grade. Patients with high CLC-3 expression had an overall shorter survival time, whereas patients with low expression of CLC-3 had a better survival time. Silencing endogenous CLC-3 with ShCLC-3 adenovirus significantly decreases volume-regulated chloride currents, inhibits the nuclear translocation of p65 subunit of Nuclear Factor-κB (NF-κB), decreases transcriptional activity of NF-κB, reduces MMP-3 and MMP-9 expression and decreases glioma cell migration and invasion. Taken together, these results suggest CLC-3 promotes the aggressiveness of glioma at least in part through nuclear factor-κB pathway, and might be a novel prognostic biomarker and therapeutic target for glioma.

Indexed as

CLC-3gliomainvasionmatrix metalloproteinasenuclear factor-κB

Identifiers

PMID28969029
PMCPMC5609961
OpenAlexW2724132241

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.