Evidence map›Paper›PMID 28187000›Full record

ArticleOncotarget2017

MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.

Wei Chen, Xin-Ke Xu, Jun-Liang Li, Kuan-Kei Kong, Hui Li, Cheng Chen, Jing He, Fangyu Wang, Ping Li, Xiao-Song Ge and 1 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

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27 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 1 country.

Wei ChenDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Xin-Ke XuDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Jun-Liang LiDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Kuan-Kei KongDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Hui LiDepartment of Respiratory, The First People's Hospital of Foshan, Sun Yat-Sen University, Guangdong Foshan 528000, China.
Cheng ChenDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Jing HeDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Fangyu WangDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Ping LiDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Xiao-Song GeDepartment of Oncology, The Affiliated Hospital of Jiangnan University, Wuxi 214062, Jiangsu, China.
Fang-Cheng LiDepartment of Neurosurgery, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.
Guangzhou Medical University · CNSun Yat-sen Memorial Hospital · CNChinese Academy of Sciences · CNFirst People's Hospital of Foshan · CNWuxi Fourth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most malignant brain tumor with limited therapeutic options. Temozolomide (TMZ) is a novel cytotoxic agent used as first-line chemotherapy for GBM, however, some individual cells can't be isolated for surgical resection and show treatment-resistance, thus inducing poor prognosis. By using the HiSeq sequencing and bioinformatics methods, we identified lncRNAs showing different expression levels in TMZ-resistant and non-resistant patients. RT-qPCR was then performed in tissues and serum samples, and lncRNA MALAT1 was finally identified to show considerable discriminating potential to identify responding patients from non-responding patients. Moreover, high serum MALAT1 expression was associated with poor chemoresponse and survival in GBM patients receiving TMZ treatment. Subsequently, the TMZ resistant cell lines were established, and the CCK8 assay showed that lncRNA MALAT1 knockdown significantly reversed TMZ resistance in GBM cells. The gain and loss-function experiments revealed that miR-203 was down-regulated by MALAT1 and this interaction has reciprocal effects. Besides, thymidylate synthase (TS) mRNA was identified as a direct target of miR-203. LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression. In conclusion, our integrated approach demonstrates that enhanced expression of lncRNA MALAT1 confers a potent poor therapeutic efficacy and inhibition of MALAT1 levels could be a future direction to develop a novel therapeutic strategy to overcome TMZ resistance in GBM patients.

Indexed as

Antineoplastic Agents, AlkylatingApoptosisBiomarkers, TumorBrain NeoplasmsCell CycleCell ProliferationDacarbazineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGlioblastomaHumansMicroRNAsNeoplasm StagingPrognosisRNA, Long NoncodingSurvival RateAntineoplastic Agents, AlkylatingBiomarkers, TumorDacarbazineMALAT1 long non-coding RNA, humanMicroRNAsMIRN203 microRNA, humanRNA, Long NoncodingTemozolomideThymidylate SynthasechemoresistanceMALAT1miR-203temozolomidethymidylate synthase

Identifiers

PMID28187000
PMCPMC5410262
OpenAlexW2588834106

What OpenQuestion holds

Textmetadata
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.