Evidence map›Paper›PMID 35032258›Full record

ArticleMolecular biology reports2022

TRIP13 knockdown inhibits the proliferation, migration, invasion, and promotes apoptosis by suppressing PI3K/AKT signaling pathway in U2OS cells.

De-Chen Yu, Xiang-Yi Chen, Hai-Yu Zhou, De-Quan Yu, Xiao-Lei Yu, Yi-Cun Hu, Rui-Hao Zhang, Xiao-Bo Zhang, Kun Zhang, Mao-Qiang Lin and 2 more

Abstract read
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In one paragraph

Article in Molecular biology reports, 2022. 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
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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

De-Chen Yu *Department of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Xiang-Yi Chen *Department of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Hai-Yu ZhouDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China. zhouhy@lzu.edu.cn.ORCID http://orcid.org/0000-0001-8722-3773
De-Quan YuDepartment of Radiotherapy, Air Force Medical University Tangdu Hospital, 710000, Xi'an, China.
Xiao-Lei YuDepartment of cardiology, Air Force Medical University Tangdu Hospital, 710000, Xi'an, China.
Yi-Cun HuDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Rui-Hao ZhangDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Xiao-Bo ZhangDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Kun ZhangDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Mao-Qiang LinDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Xi-Dan GaoDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Tao-Wen GuoDepartment of Orthopedics, Lanzhou University Second Hospital, 730000, Lanzhou, China.
Lanzhou University Second Hospital · CNAir Force Medical University · CN

Funding

Lanzhou Science and Technology Bureau 2018-3-79
6 · The paper itself

Abstract

backgroundAlthough osteosarcoma (OS) is the most common malignant bone tumor, the biological mechanism underlying its incidence and improvement remains unclear. This study investigated early diagnosis and treatment objectives using bioinformatics strategies and performed experimental verification. METHODS AND

resultsThe top 10 OS hub genes-CCNA2, CCNB1, AURKA, TRIP13, RFC4, DLGAP5, NDC80, CDC20, CDK1, and KIF20A-were screened using bioinformatics methods. TRIP13 was chosen for validation after reviewing literature. TRIP13 was shown to be substantially expressed in OS tissues and cells, according to Western blotting (WB) and quantitative real-time polymerase chain reaction data. Subsequently, TRIP13 knockdown enhanced apoptosis and decreased proliferation, migration, and invasion in U2OS cells, as validated by the cell counting kit-8 test, Hoechst 33,258 staining, wound healing assay, and WB. In addition, the levels of p-PI3K/PI3K and p-AKT/AKT in U2OS cells markedly decreased after TRIP13 knockdown. Culturing U2OS cells, in which TRIP13 expression was downregulated, in a medium supplemented with a PI3K/AKT inhibitor further reduced their proliferation, migration, and invasion and increased their apoptosis.

conclusionsTRIP13 knockdown reduced U2OS cell proliferation, migration, and invasion via a possible mechanism involving the PI3K/AKT signaling pathway.

Indexed as

Bone NeoplasmsCell Cycle ProteinsOsteosarcomaApoptosisATPases Associated with Diverse Cellular ActivitiesCell Line, TumorCell MovementCell ProliferationHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionATPases Associated with Diverse Cellular ActivitiesCell Cycle ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTRIP13 protein, humanBioinformaticsOsteosarcomaPI3K/AKT signaling pathwayThyroid hormone receptor interacting protein 13U2OS

Identifiers

PMID35032258
OpenAlexW4205674678

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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.