Evidence map›Paper›PMID 28754121›Full record

ArticleJournal of translational medicine2017

Coiled-coil domain containing 109B is a HIF1α-regulated gene critical for progression of human gliomas.

Ran Xu, Mingzhi Han, Yangyang Xu, Xin Zhang, Chao Zhang, Di Zhang, Jianxiong Ji, Yuzhen Wei, Shuai Wang, Bin Huang and 7 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
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  11. Mitochondrial CaCells · 2021
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  16. PDGFA/PDGFRα-regulated GOLM1 promotes human glioma progression through activation of AKT.Journal of experimental & clinical cancer research : CR · 2017
    Article
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

17 authors at 4 institutions in 2 countries.

Ran XuDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Mingzhi HanDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Yangyang 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.
Chao ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Di ZhangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Jianxiong JiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Yuzhen 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.
Bin HuangDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Anjing ChenDepartment 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.
Wenjie LiDepartment of Neurosurgery, Qilu Hospital of Shandong University and Brain Science Research Institute, Shandong University, #107 Wenhua Xi Road, Jinan, 250012, China.
Tao SunNingxia Key Laboratory of Craniocerebral Diseases, Incubation Base of the National Key Laboratory, Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Feng WangNingxia Key Laboratory of Craniocerebral Diseases, Incubation Base of the National Key Laboratory, Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Xingang 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 · CNNingxia Medical University · CNJining First People's Hospital · CNUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe coiled-coil domain is a structural motif found in proteins that participate in a variety of biological processes. Aberrant expression of such proteins has been shown to be associated with the malignant behavior of human cancers. In this study, we investigated the role of a specific family member, coiled-coil domain containing 109B (CCDC109B), in human gliomas. METHODS AND

resultsWe confirmed that CCDC109B was highly expressed in high grade gliomas (HGG; WHO III-IV) using immunofluorescence, western blot analysis, immunohistochemistry (IHC) and open databases. Through Cox regression analysis of The Cancer Genome Atlas (TCGA) database, we found that the expression levels of CCDC109B were inversely correlated with patient overall survival and it could serve as a prognostic marker. Then, a serious of cell functional assays were performed in human glioma cell lines, U87MG and U251, which indicated that silencing of CCDC109B attenuated glioma proliferation and migration/invasion both in vitro and in vivo. Notably, IHC staining in primary glioma samples interestingly revealed localization of elevated CCDC109B expression in necrotic areas which are typically hypoxic. Moreover, small interfering RNA (siRNA) and specific inhibiters of HIF1α led to decreased expression of CCDC109B in vitro and in vivo. Transwell assay further showed that CCDC109B is a critical factor in mediating HIF1α-induced glioma cell migration and invasion.

conclusionOur study elucidated a role for CCDC109B as an oncogene and a prognostic marker in human gliomas. CCDC109B may provide a novel therapeutic target for the treatment of human glioma.

Indexed as

AnimalsBiomarkers, TumorBrain NeoplasmsCell HypoxiaCell MovementCell ProliferationDisease ProgressionFemaleGene Knockdown TechniquesGliomaHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMembrane ProteinsMice, NudeMiddle AgedBiomarkers, TumorHypoxia-Inducible Factor 1, alpha SubunitMCUB protein, humanMembrane ProteinsMitochondrial ProteinsCCDC109BGliomaHIF1αInvasionProliferation

Identifiers

PMID28754121
PMCPMC5534085
OpenAlexW2742094821

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.