Evidence map›Paper›PMID 35322916›Full record

ArticleJournal of cellular and molecular medicine2022

Evaluation of the TRIP13 level in breast cancer and insights into potential molecular pathways.

Jin Lan, Jingzhan Huang, Xinyi Tao, Yuan Gao, Longshan Zhang, Weiqiang Huang, Junjie Luo, Chuqin Liu, Yunyao Deng, Lixin Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 24 citations in OpenAlex.

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  12. Role of TRIP13 in human cancer development.Molecular biology reports · 2024
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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

11 authors at 2 institutions in 1 country.

Jin LanDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Jingzhan HuangDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Xinyi TaoDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Yuan GaoDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Longshan ZhangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Weiqiang HuangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Junjie LuoDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Chuqin LiuDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Yunyao DengDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Lixin LiuDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Xiaolong LiuDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.ORCID 0000-0002-5899-6563
Third Affiliated Hospital of Southern Medical University · CNNanfang Hospital · CN

Funding

Science and Technology Plan Project of Guangzhou City 202002030020
6 · The paper itself

Abstract

TRIP13 is a member of the large superfamily of the AAA + ATPase proteins and is associated with a variety of activities. Emerging evidence has shown that TRIP13 may serve as an oncogene. However, the function of TRIP13 in breast cancer (BC) has not yet been elucidated. Here, a variety of bioinformatic tools and laboratory experiments were combined to analyse the expression patterns, prognostic value and functional network of TRIP13 in BC. Multiple databases and immunohistochemistry (IHC) indicated a higher TRIP13 expression in BC tissue compared with normal tissue. TRIP13 was highly expressed in lung metastatic lesions compared with primary tumours in a 4T1 cell implantation BALB/c mouse model of BC. Kaplan-Meier plots also revealed that high TRIP13 expression correlated with poor survival in patients with BC. Furthermore, gene set enrichment analysis revealed that TRIP13 was primarily enriched in the signalling pathway of PI3K-AKT-mTOR. Suppressing TRIP13 could inhibit the expression of related genes, as well as the proliferation and migration of BC cell. Finally, 10 hub genes with a high score of connectivity were filtered from the protein-protein interaction (PPI) network, including MAD2L1, CDC20, CDC5L, CDK1, CCNA2, BUB1B, RAD51, SPO11, KIF11 and AURKB. Thus, TRIP13 may be a promising prognostic biomarker and an effective therapeutic target for BC.

Indexed as

Breast NeoplasmsAnimalsATPases Associated with Diverse Cellular ActivitiesBiomarkers, TumorCell Cycle ProteinsFemaleGene Expression Regulation, NeoplasticHumansMicePhosphatidylinositol 3-KinasesRNA-Binding ProteinsSignal TransductionATPases Associated with Diverse Cellular ActivitiesBiomarkers, TumorCDC5L protein, humanCell Cycle ProteinsPhosphatidylinositol 3-KinasesRNA-Binding ProteinsTRIP13 protein, humanbreast cancercell proliferationprognosistherapeutic targetTRIP13

Identifiers

PMID35322916
PMCPMC9077308
OpenAlexW4220671256

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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.