Evidence map›Paper›PMID 28977927›Full record

ArticleOncotarget2017

TRIM22 confers poor prognosis and promotes epithelial-mesenchymal transition through regulation of AKT/GSK3β/β-catenin signaling in non-small cell lung cancer.

Li Liu, Xiao-Ming Zhou, Fang-Fei Yang, Yuan Miao, Yan Yin, Xue-Jun Hu, Gang Hou, Qiu-Yue Wang, Jian Kang

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 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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  11. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
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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

9 authors at 2 institutions in 1 country.

Li LiuDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Xiao-Ming ZhouDepartment of Respiratory Medicine, The Shengjing Hospital of China Medical University, Shenyang 110004, China.
Fang-Fei YangDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Yuan MiaoDepartment of Pathology, The First Hospital and College of Basic Medical Sciences, China Medical University, Shenyang 110001, China.
Yan YinDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Xue-Jun HuDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Gang HouDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Qiu-Yue WangDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
Jian KangDepartment of Respiratory Medicine, The First Hospital of China Medical University, Shenyang 110001, China.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression pattern and biological roles of TRIM22 remains unknown in most human cancers. The present study aims to discover its clinical significance and function in human non-small cell lung cancer (NSCLC). Immunohistochemistry was used to examine TRIM22 expression in 126 cases of NSCLC specimens. TRIM22 protein was upregulated in 70/126 (55.6%) non-small cell lung cancer tissues compared with normal lung tissue. TRIM22 overexpression was associated with advanced TNM stage, positive nodal metastasis and poor prognosis. Plasmid and siRNA transfection were performed in lung cancer cell lines. TRIM22 overexpression promoted proliferation, colony formation and invasion in A549 cells. While its depletion exhibited the opposite effects in H1299 cell line. TRIM22 overexpression promoted cell cycle progression through regulation of cyclin D1, cyclin E and p27. TRIM22 also changed the expression of epithelial to mesenchymal transition (EMT) markers including E-cadherin N-cadherin, Vimentin and Snail. Furthermore, TRIM22 activated PI3K/AKT/GSK3β/β-catenin oncogenic signaling pathways. Treatment with PI3K inhibitor LY294002 and β-catenin siRNA blocked the effects of TRIM22 on EMT in TRIM22-overexpressing cells. In conclusion,TRIM22 serves as an important oncoprotein and a promoter of cell proliferation and invasion through AKT/ GSK3β/β-catenin induced EMT in NSCLC.

Indexed as

invasionnon-small cell lung cancerprognosisproliferationTRIM22

Identifiers

PMID28977927
PMCPMC5617487
OpenAlexW2731318226

What OpenQuestion holds

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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.