Evidence map›Paper›PMID 31740732›Full record

ArticleBritish journal of cancer2019

TRIP13 promotes the cell proliferation, migration and invasion of glioblastoma through the FBXW7/c-MYC axis.

Guanghui Zhang, Qingzong Zhu, Gang Fu, Jianbing Hou, Xiaosong Hu, Jiangjun Cao, Wen Peng, Xiaowen Wang, Fei Chen, Hongjuan Cui

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.7field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 99 citations in OpenAlex.

  1. DamageZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  5. Role of TRIP13 in human cancer development.Molecular biology reports · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Guanghui ZhangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Qingzong ZhuState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Gang FuDental Hospital Affiliated to Chongqing Medical University, Chongqing, 400016, China.
Jianbing HouState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Xiaosong HuState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Jiangjun CaoState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Wen PengState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Xiaowen WangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.
Fei ChenDepartment of Pharmaceutical Sciences EACPHS, Wayne State University 259 Mack Avenue, Detroit, MI, 48201, USA.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China. hcui@swu.edu.cn.
State Key Laboratory of Silkworm Genomic BiologySouthwest University · CNChongqing Medical University · CNEugene Applebaum College of Pharmacy and Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThyroid hormone receptor interactor 13 (TRIP13) is an AAA + ATPase that plays an important role in the mitotic checkpoint. TRIP13 is highly expressed in various human tumours and promotes tumorigenesis. However, the biological effect of TRIP13 in GBM cells remains unclear.

methodsWe generated GBM cell models with overexpressed or silenced TRIP13 via lentivirus-mediated overexpression and RNAi methods. The biological role of TRIP13 in the proliferation, migration and invasion of GBM cells has been further explored.

resultsOur research indicated that TRIP13 was highly expressed in GBM tissues and cells. We found that the proliferation, migration and invasion abilities were inhibited in TRIP13-knockdown GBM cells. These results indicated that TRIP13 plays an important role in the tumorigenesis of GBM. Moreover, we found that TRIP13 first stabilised c-MYC by inhibiting the transcription of FBXW7, which is an E3 ubiquitin ligase of c-MYC, by directly binding to the promoter region of FBXW7. Therefore, our study indicated that the TRIP13/FBXW7/c-MYC pathway might provide a prospective therapeutic target in the treatment of GBM.

conclusionsThese results indicated that TRIP13 plays an oncogenic role in GBM. The TRIP13/FBXW7/c-MYC pathway might act as a prospective therapeutic target for GBM patients.

Indexed as

AdultAgedApoptosisATPases Associated with Diverse Cellular ActivitiesCarcinogenesisCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDisease-Free SurvivalF-Box-WD Repeat-Containing Protein 7FemaleGene Expression Regulation, NeoplasticGlioblastomaHumansKaplan-Meier EstimateATPases Associated with Diverse Cellular ActivitiesCell Cycle ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMYC protein, humanProto-Oncogene Proteins c-mycTRIP13 protein, human

Identifiers

PMID31740732
PMCPMC6964669
OpenAlexW2983237237

What OpenQuestion holds

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Registered trials

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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.