Evidence map›Paper›PMID 25940705›Full record

ArticleOncotarget2015

Transcriptional co-activator TAZ sustains proliferation and tumorigenicity of neuroblastoma by targeting CTGF and PDGF-β.

Mei Wang, Yang Liu, Jiahua Zou, Rui Yang, Fan Xuan, Yi Wang, Ning Gao, Hongjuan Cui

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

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  8. Identification of neuroblastoma cell lines with uncommon TAZJournal for immunotherapy of cancer · 2021
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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

8 authors at 5 institutions in 1 country.

Mei WangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Yang LiuDepartment of Respiration, the Third Hospital of Hebei Medical University, Shijiazhuang, China.
Jiahua ZouState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Rui YangState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Fan XuanState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
Yi WangCardiovascular Department, Second Affiliated Hospital of University of South China, Hengyang, China.
Ning GaoDepartment of Pharmacognosy, College of Pharmacy, Third Military Medical University, Chongqing, China.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China.
State Key Laboratory of Silkworm Genomic BiologySouthwest University · CNArmy Medical University · CNHebei Medical University · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma is a common childhood malignant tumor originated from the neural crest-derived sympathetic nervous system. A crucial event in the pathogenesis of neuroblastoma is to promote proliferation of neuroblasts, which is closely related to poor survival. However, mechanisms for regulation of cell proliferation and tumorigenicity in neuroblastoma are not well understood. Here, we report that overexpression of TAZ in neuroblastoma BE(2)-C cells causes increases in cell proliferation, self renewal and colony formation, which was restored back to its original levels by knockdown of TAZ in TAZ-overexpression cells. Inhibition of endogenous TAZ attenuated cell proliferation, colony formation and tumor development in neuroblastoma SK-N-AS cell, which could be rescued by re-introduction of TAZ into TAZ-knockdown cells. In addition, we found that overexpressing TAZ-mediated induction of CTGF and PDGF-β expression, cell proliferation and colony formation were inhibited by knocking down CTGF and PDGF-β with siRNA in TAZ-overexpressing cell. Overall, our findings suggested that TAZ plays an essential role in regulating cell proliferation and tumorigenesis in neuroblastoma cells. Thus, TAZ seems to be a novel and promising target for the treatment of neuroblastoma.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell AdhesionCell DivisionCell Line, TumorConnective Tissue Growth FactorGenes, sisHeterograftsHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred NODMice, SCIDMolecular Targeted TherapyNeoplasm ProteinsNeuroblastomaCCN2 protein, humanConnective Tissue Growth FactorIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsProto-Oncogene Proteins c-sisRecombinant Fusion ProteinsRNA, Small InterferingTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humancell proliferationcolony formationneuroblastomaTAZ

Identifiers

PMID25940705
PMCPMC4496235
OpenAlexW1950329111

What OpenQuestion holds

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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.