Evidence map›Paper›PMID 27998273›Full record

ArticleJournal of translational medicine2016

LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2.

Xin Wang, Lalit Sehgal, Neeraj Jain, Tamer Khashab, Rohit Mathur, Felipe Samaniego

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

68 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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8 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

6 authors.

Xin WangDepartment of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lalit SehgalDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. lsehgal@mdanderson.org.
Neeraj JainDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA.
Tamer KhashabDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA.
Rohit MathurDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA.
Felipe SamaniegoDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, 77030, USA. fsamaniego@mdanderson.org.

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
PMLRARalpha and PML directly regulate Fas-mediated apoptosis in vivoR21CA158692 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SAMANIEGO, FELIPE · 2011 to 2012
$378k
NCI NIH HHS P30 CA016672NCI NIH HHS R21 CA158692
6 · The paper itself

Abstract

backgroundMantle cell lymphoma (MCL) is considered an aggressive subtype of non-Hodgkin's lymphoma with variable treatment responses. There is an urgent need to identify novel markers with prognostic and therapeutic value for MCL. Long non-coding RNAs (lncRNAs) have emerged as key regulators in cancers, including MCL. Metastasis-associated lung adenocarcinoma transcript 1(MALAT1), a lncRNA located at pathognomonic translocation site of t (11; 14) of MCL. MALAT1 is known to be overexpressed in solid tumors and hematologic malignancies. However, the pathological role and clinical relevance of MALAT1 in MCL are not completely understood.

methodsWe quantified MALAT1 in MCL samples (40) and CD19+ B cells by quantitative real time polymerase chain reaction (qRT-PCR) and correlated levels with clinical outcome. We silenced MALAT1 in MCL cell lines and analyzed cells in tumorigenic assays and formation of transcription complexes.

resultsWe found that the expression of MALAT1 was elevated in human MCL tumors and cell lines as compared to normal controls, and the elevated levels of MALAT1 correlated with higher MCL international prognostic index (MIPI) and reduced overall survival. MCL with knockdown of MALAT1 showed impaired cell proliferation, facilitated apoptosis and produced fewer clonogenic foci. The increased expression of p21 and p27 upon MALAT1 knockdown was regulated by enhancer of zeste homolog 2 (EZH2). Moreover, decreased phosphorylation of EZH2 at T350 attenuated the binding to MALAT1.

conclusionsOur findings illuminate the oncogenic role of MALAT1, which may serve as a novel biomarker and as a therapeutic target in MCL.

Indexed as

ApoptosisCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Enhancer of Zeste Homolog 2 ProteinGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLymphoma, Mantle-CellModels, BiologicalPhosphorylationPolycomb Repressive Complex 2Protein BindingRNA, Long NoncodingCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Enhancer of Zeste Homolog 2 ProteinMALAT1 long non-coding RNA, humanPolycomb Repressive Complex 2RNA, Long NoncodingCell cycleEZH2Long non-coding RNAMALAT1MCLPhosphorylation

Identifiers

PMID27998273
PMCPMC5175387

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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.