Evidence map›Paper›PMID 31430050›Full record

ArticleJournal of cellular and molecular medicine2019

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF-κB positive feedback loop.

Yiming Tu, Peng Xie, Xiaoliu Du, Liang Fan, Zhongyuan Bao, Guangchi Sun, Pengzhan Zhao, Honglu Chao, Chong Li, Ailiang Zeng and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-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

39 citing papers in PubMed, 64 citations in OpenAlex.

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  16. Prognostic Value of S100 Family mRNA Expression in Hepatocellular Carcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 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

12 authors at 3 institutions in 2 countries.

Yiming TuDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-5870-7717
Peng XieDepartment of Neurosurgery, The Affiliated Huai'an Hospital of Xuzhou Medical University, The Second People's Hospital of Huai'an, Huai'an, China.
Xiaoliu DuDepartment of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liang FanDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhongyuan BaoDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Guangchi SunDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Pengzhan ZhaoDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Honglu ChaoDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Chong LiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ailiang ZengDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Minhong PanDepartment of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jing JiDepartment of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CNBrigham and Women's Hospital · USXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up-regulated in GBM tissues and higher S100A11 expression indicated poor prognosis of GBM patients. Overexpression of S100A11 promoted GBM cell growth, epithelial-mesenchymal transition (EMT), migration, invasion and generation of glioma stem cells (GSCs), whereas its knockdown inhibited these activities. More importantly, S100A11 interacted with ANXA2 and regulated NF-κB signalling pathway through decreasing ubiquitination and degradation of ANXA2. Additionally, NF-κB regulated S100A11 at transcriptional level as a positive feedback. We also demonstrated the S100A11 on tumour growth in GBM using an orthotopic tumour xenografting. These data demonstrate that S100A11/ANXA2/NF-κB positive feedback loop in GBM cells that promote the progression of GBM.

Indexed as

Feedback, PhysiologicalOncogenesAnimalsAnnexin A2Brain NeoplasmsCarcinogenesisCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlioblastomaHumansMaleMice, Inbred BALB CMice, NudeAnnexin A2NF-kappa BProteasome Endopeptidase ComplexS100A11 protein, humanS100 ProteinsANXA2glioblastomaNF-κBS100A11ubiquitination

Identifiers

PMID31430050
PMCPMC6787445
OpenAlexW2969665415

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.