Evidence map›Paper›PMID 30848088›Full record

ArticleCancer medicine2019

Pard3 suppresses glioma invasion by regulating RhoA through atypical protein kinase C/NF-κB signaling.

Junjun Li, Hao Xu, Qiangping Wang, Peng Fu, Tao Huang, Omarkhalil Anas, Hongyang Zhao, Nanxiang Xiong

RetractedOpen access · goldAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 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 It has been retracted, and should not be counted.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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. RNF7 promotes glioma growth via the PI3K/AKT signalling axis.Journal of cellular and molecular medicine · 2023
    Article
  8. Article
  9. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Junjun LiDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Hao XuDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Qiangping WangDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Peng FuDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Tao HuangDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Omarkhalil AnasSection of Histology and Embryology, Department of Anatomy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Hongyang ZhaoDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Nanxiang XiongDepartment of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.ORCID 0000-0001-5306-1155
Union Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Partitioning defective protein 3 (Pard3) has been reported to inhibit the progression of numerous human cancer cell types. However, the role of Pard3 in glioma progression remains unclear. In this study, the expression of Pard3 was measured in human gliomas of different grades by both quantitative polymerase chain reaction and Western blotting. The effect of Pard3 on glioma progression was tested using cell counting kit-8 assays, EdU assays, colony formation assays, cell migration, and invasion assays and tumor xenografts. The effect of Pard3 on Ras homolog family member A (RhoA) protein levels, subcellular localization, and transcriptional activity was measured by immunoblotting and immunofluorescence. Our results indicate that Pard3 functions as a tumor suppressor in gliomas and that the loss of Pard3 protein is strongly associated with a higher grade and poorer outcome. Pard3 overexpression inhibits glioma progression by upregulating RhoA protein levels. However, the level of GTP-RhoA protein remained unchanged. Further evidence demonstrates that Pard3 regulates RhoA protein levels, subcellular localization and transcriptional activity by activating atypical protein kinase C/NF-κB signaling. Mouse modeling experiments show that Pard3 overexpression inhibits glioma cell growth in vivo. Taken together, these findings identify RhoA as a novel target of Pard3 in gliomas and substantiate a novel regulatory role for Pard3 in glioma progression. This study reveals that Pard3 plays an inhibitory role in gliomas by regulating RhoA, which reveals a potential benefit for Pard3 activators in the prevention and therapy of gliomas.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingAdultAgedAnimalsBrain NeoplasmsCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticComputational BiologyDisease Models, AnimalFemaleGene ExpressionGene Expression ProfilingAdaptor Proteins, Signal TransducingCell Cycle ProteinsNF-kappa BPARD3 protein, humanPKC-3 proteinProtein Kinase CrhoA GTP-Binding ProteinRHOA protein, humangliomasinvasionPard3RhoAtumor recurrence

Identifiers

PMID30848088
PMCPMC6536976
OpenAlexW2921566266

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.