Evidence map›Paper›PMID 28548934›Full record

ArticleOncotarget2017

IKBKE regulates cell proliferation and epithelial-mesenchymal transition of human malignant glioma via the Hippo pathway.

Jie Lu, Yi Yang, Gaochao Guo, Yang Liu, Zhimeng Zhang, Shicai Dong, Yang Nan, Zhenyi Zhao, Yue Zhong, Qiang Huang

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 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. TEAD4 as an Oncogene and a Mitochondrial Modulator.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. IKBKE enhances TMZ-chemoresistance through upregulation of MGMT expression in glioblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. IKBKE inhibits TSC1 to activate the mTOR/S6K pathway for oncogenic transformation.Turkish journal of biology = Turk biyoloji dergisi · 2018
    Article
  20. 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

10 authors at 2 institutions in 1 country.

Jie LuDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Yi YangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Gaochao GuoDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Yang LiuDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Zhimeng ZhangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Shicai DongDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Yang NanDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Zhenyi ZhaoDepartment of Neurosurgery, Tianjin Baodi People's Hospital, Baodi District, Tianjin 301800, China.
Yue ZhongDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Qiang HuangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China.
Tianjin Medical University General Hospital · CNTianjin People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IKBKE is increased in several types of cancers and is associated with tumour malignancy. In this study, we confirmed that IKBKE promoted glioma proliferation, migration and invasion in vitro. Then, we further discovered that IKBKE increased Yes-associated protein 1 (YAP1) and TEA domain family member 2 (TEAD2), two important Hippo pathway downstream factors, to induce an epithelial-mesenchymal transition (EMT), thus contributing to tumour invasion and metastasis. We also testified that YAP1 and TEAD2 promoted epithelial-mesenchymal transition (EMT) in malignant glioma. Furthermore, we constructed nude mouse subcutaneous and intracranial models to verify that IKBKE could attenuate U87-MG tumourigenicity in vivo. Collectively, our results suggest that IKBKE plays a pivotal role in regulating cell proliferation, invasion and epithelial-mesenchymal transition of malignant glioma cells in vitro and in vivo by impacting on the Hippo pathway. Therefore, targeting IKBKE may become a new strategy to treat malignant glioma.

Indexed as

Signal TransductionAnimalsATP Binding Cassette Transporter, Subfamily B, Member 2Cell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalDNA-Binding ProteinsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene SilencingGliomaHeterograftsHippo Signaling PathwayATP Binding Cassette Transporter, Subfamily B, Member 2DNA-Binding ProteinsI-kappa B KinaseIKBKE protein, humanProtein Serine-Threonine KinasesTEAD2 protein, humanTEA Domain Transcription FactorsTranscription Factorsepithelial–mesenchymal transition (EMT)gliomaHippo pathwayIKBKE

Identifiers

PMID28548934
PMCPMC5564784
OpenAlexW2613957075

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.