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

Overview of attention for article published in Journal of Translational Medicine, December 2016
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About this Attention Score

  • Good Attention Score compared to outputs of the same age (65th percentile)
  • Good Attention Score compared to outputs of the same age and source (74th percentile)

Mentioned by

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1 tweeter
patent
1 patent

Citations

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66 Dimensions

Readers on

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53 Mendeley
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Title
LncRNA MALAT1 promotes development of mantle cell lymphoma by associating with EZH2
Published in
Journal of Translational Medicine, December 2016
DOI 10.1186/s12967-016-1100-9
Pubmed ID
Authors

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

Abstract

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

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 53 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Sweden 1 2%
Unknown 52 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 21%
Student > Bachelor 9 17%
Student > Master 6 11%
Other 5 9%
Student > Doctoral Student 5 9%
Other 8 15%
Unknown 9 17%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 17 32%
Agricultural and Biological Sciences 8 15%
Medicine and Dentistry 6 11%
Nursing and Health Professions 2 4%
Computer Science 2 4%
Other 6 11%
Unknown 12 23%

Attention Score in Context

This research output has an Altmetric Attention Score of 4. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 March 2021.
All research outputs
#6,418,231
of 20,439,515 outputs
Outputs from Journal of Translational Medicine
#1,014
of 3,571 outputs
Outputs of similar age
#138,918
of 410,887 outputs
Outputs of similar age from Journal of Translational Medicine
#76
of 331 outputs
Altmetric has tracked 20,439,515 research outputs across all sources so far. This one has received more attention than most of these and is in the 67th percentile.
So far Altmetric has tracked 3,571 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.8. This one has gotten more attention than average, scoring higher than 70% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 410,887 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 65% of its contemporaries.
We're also able to compare this research output to 331 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 74% of its contemporaries.