Evidence map›Paper›PMID 29110682›Full record

ArticleJournal of experimental & clinical cancer research : CR2017

TAGLN2 is a candidate prognostic biomarker promoting tumorigenesis in human gliomas.

Ming-Zhi Han, Ran Xu, Yang-Yang Xu, Xin Zhang, Shi-Lei Ni, Bin Huang, An-Jing Chen, Yu-Zhen Wei, Shuai Wang, Wen-Jie Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 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

14 authors at 2 institutions in 2 countries.

Ming-Zhi HanDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Ran XuDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Yang-Yang XuDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Xin ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Shi-Lei NiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Bin HuangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
An-Jing ChenDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Yu-Zhen WeiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Shuai WangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Wen-Jie LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Qing ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Gang LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Xin-Gang LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China. lixg@sdu.edu.cn.
Jian WangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China. jian.wang@uib.no.
Qilu Hospital of Shandong University · CNUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransgelin-2 (TAGLN2) is a member of the calponin family of actin-bundling proteins that is involved in the regulation of cell morphology, motility, and cell transformation. Here, the clinical significance and potential function of TAGLN2 in malignant gliomas were investigated.

methodsMolecular and clinical data was obtained from The Cancer Genome Atlas (TCGA) database. Gene ontology and pathway analysis was used to predict potential functions of TAGLN2. RNA knockdown was performed using siRNA or lentiviral contructs in U87MG and U251 glioma cell lines. Cells were characterized in vitro or implanted in vivo to generate orthotopic xenografts in order to assess molecular status, cell proliferation/survival, and invasion by Western blotting, flow cytometry, and 3D tumor spheroid invasion assay, respectively.

resultsIncreased TAGLN2 expression was associated with increasing tumor grade (P < 0.001), the mesenchymal molecular glioma subtype and worse prognosis in patients (P < 0.001). Immunohistochemistry performed with anti-TAGLN2 on an independent cohort of patients (n = 46) confirmed these results. Gene silencing of TAGLN2 in U87MG and U251 significantly inhibited invasion and tumor growth in vitro and in vivo. Western blot analysis revealed that epithelial-mesenchymal transition (EMT) molecular markers, such as N-cadherin, E-cadherin, and Snail, were regulated in a manner corresponding to suppression of the EMT phenotype in knockdown experiments. Finally, TAGLN2 was induced ~ 2 to 3-fold in U87MG and U251 cells by TGFβ2, which was also elevated in GBM and highly correlated with TAGLN2 mRNA levels (P < 0.001).

conclusionsOur findings indicate that TAGLN2 exerts a role in promoting the development of human glioma. The regulation and function of TAGLN2 therefore renders it as a candidate molecular target for the treatment of GBM.

Indexed as

Up-RegulationAnimalsBiomarkers, TumorBrain NeoplasmsCell Line, TumorCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGliomaHumansMaleMiceMicrofilament ProteinsMuscle ProteinsBiomarkers, TumorMicrofilament ProteinsMuscle ProteinsTagln2 protein, humanCell cycleEMTGliomaTAGLN2TGFβ signaling

Identifiers

PMID29110682
PMCPMC5674233
OpenAlexW2767508303

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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.