Evidence map›Paper›PMID 25638155›Full record

ArticleOncotarget2015

Cisplatin-selected resistance is associated with increased motility and stem-like properties via activation of STAT3/Snail axis in atypical teratoid/rhabdoid tumor cells.

Wei-Hsiu Liu, Ming-Teh Chen, Mong-Lien Wang, Yi-Yen Lee, Guang-Yuh Chiou, Chian-Shiu Chien, Pin-I Huang, Yi-Wei Chen, Ming-Chao Huang, Shih-Hwa Chiou and 2 more

Open access · diamondAbstract read
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 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 62 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

12 authors at 4 institutions in 1 country.

Wei-Hsiu LiuGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
Ming-Teh ChenSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Mong-Lien WangSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Yen LeeInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Guang-Yuh ChiouCollege of Biological Science and Technology, National Chiao Tung Univeristy, Taiwan.
Chian-Shiu ChienSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Pin-I HuangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Yi-Wei ChenInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Ming-Chao HuangSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Shih-Hwa ChiouSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yang-Hsin ShihSchool of Medicine, National Yang-Ming University, Taipei, Taiwan.
Hsin-I MaGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWNational Defense Medical Center · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atypical teratoid/rhabdoid tumor (ATRT) is a malignant pediatric brain tumor with great recurrence after complete surgery and chemotherapy. Here, we demonstrate that cisplatin treatment selects not only for resistance but also for a more oncogenic phenotype characterized by high self-renewal and invasive capabilities. These phenomena are likely due to STAT3 upregulatoin which occurred simultaneously with higher expression of Snail, an activator of epithelial-mesenchymal transition (EMT), in ATRT-CisR cells. STAT3 knockdown effectively suppressed Snail expression and blocked motility and invasion in ATRT-CisR cells, while overexpressing Snail reversed these effects. Chromatin immunoprecipitation assay indicated that STAT3 directly bound to Snail promoter. Moreover, STAT3 knockdown effectively suppressed cancer stem-like properties, synergistically enhanced the chemotherapeutic effect, and significantly improved survival rate in ATRT-CisR-transplanted immunocompromised mice. Finally, immunohistochemistrical analysis showed that STAT3 and Snail were coexpressed at high levels in recurrent ATRT tissues. Thus, the STAT3/Snail pathway plays an important role in oncogenic resistance, rendering cells not only drug-resistant but also increasingly oncogenic (invasion, EMT and recurrence). Therefore, the STAT3/Snail could be a target for ATRT treatment.

Indexed as

AnimalsAntineoplastic AgentsBrain NeoplasmsCell Line, TumorCell MovementCisplatinDrug Resistance, NeoplasmFemaleHeterograftsHumansMaleMiceMice, SCIDRhabdoid TumorSignal TransductionSnail Family Transcription FactorsAntineoplastic AgentsCisplatinSnail Family Transcription FactorsSTAT3 protein, humanSTAT3 Transcription FactorTranscription Factors

Identifiers

PMID25638155
PMCPMC4359329
OpenAlexW1584810294

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.