Evidence map›Paper›PMID 33725213›Full record

ArticleJournal of molecular histology2021

Upregulation of CPNE3 suppresses invasion, migration and proliferation of glioblastoma cells through FAK pathway inactivation.

Dijian Shi, Bo Lin, Jun Lai, Kaipeng Li, Yimo Feng

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  6. [High expression of CPNE3 correlates with poor long-term prognosis of gastric cancer by inhibiting cell apoptosisNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. The CPNE Family and Their Role in Cancers.Frontiers in genetics · 2021
    Review
  11. Article
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

5 authors at 1 institution in 1 country.

Dijian ShiDepartment of Neurosurgery, Chongqing General Hospital, University of Chinese Academy of Science, 118 Xingguang Avenue, Liangjiang New Area, Chongqing, 400016, China.
Bo LinDepartment of Neurosurgery, Chongqing General Hospital, University of Chinese Academy of Science, 118 Xingguang Avenue, Liangjiang New Area, Chongqing, 400016, China.
Jun LaiDepartment of Neurosurgery, Chongqing General Hospital, University of Chinese Academy of Science, 118 Xingguang Avenue, Liangjiang New Area, Chongqing, 400016, China.
Kaipeng LiDepartment of Neurosurgery, Chongqing General Hospital, University of Chinese Academy of Science, 118 Xingguang Avenue, Liangjiang New Area, Chongqing, 400016, China.
Yimo FengDepartment of Neurosurgery, Chongqing General Hospital, University of Chinese Academy of Science, 118 Xingguang Avenue, Liangjiang New Area, Chongqing, 400016, China. kongkong2020@tom.com.
First People's Hospital of Chongqing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is a deadly brain tumor with a bleak prognosis. In recent years, the copine III (CPNE3) protein was discovered to be associated to metastasis across various types of malignancies. Nevertheless, its function has not been well documented in glioma. This study characterizes CPNE3 expression in GBM along with its impact and underlying molecular mechanism with regards to cellular migration, invasion and proliferation. Immunohistochemistry was used to characterizes CPNE3 expression in the glioma tissues. Then, knockdown of CPNE3 expression was used to analyze the role of CPNE3 in GBM cell viability, migration, invasion. Western blot analysis was performed to measure the protein levels of FAK signaling pathway. We found that GBM tissues had higher CPNE3 expressions as compared to those in normal brain tissues. CPNE3 silencing in GBM cells impaired the migratory, invasive and proliferative abilities of GBM cells that can be attributed to inactivation of the FAK signaling pathway. Collectively, these findings highlight the role of CPNE3 as a new biomarker, offering deeper insights into its carcinogenic role in GBM.

Indexed as

Signal TransductionAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell ProliferationFocal Adhesion Protein-Tyrosine KinasesGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansMiceMice, NudeNeoplasm InvasivenessPhosphoproteinsRNA, Small Interferingcopine IIIFocal Adhesion Protein-Tyrosine KinasesPhosphoproteinsRNA, Small InterferingCPNE3FAK signaling pathwayGlioblastomaInvasion

Identifiers

PMID33725213
OpenAlexW3138542780

What OpenQuestion holds

Textmetadata
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.