Evidence map›Paper›PMID 26335021›Full record

ArticleBMC genomics2015

Malat1 as an evolutionarily conserved lncRNA, plays a positive role in regulating proliferation and maintaining undifferentiated status of early-stage hematopoietic cells.

Xian-Yong Ma, Jian-Hui Wang, Jing-Lan Wang, Charles X Ma, Xiao-Chun Wang, Feng-Song Liu

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
6.4field-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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
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  8. Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025
    Article
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  13. Genes · 2024
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15 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 at 4 institutions in 2 countries.

Xian-Yong MaDepartment of Pathology, Yale University School of Medicine, New Haven, USA. xian-yong.ma@yale.edu.
Jian-Hui WangDepartment of Pathology, Yale University School of Medicine, New Haven, USA. jianhui.wang@yale.edu.
Jing-Lan WangDepartment of Pathology, Yale University School of Medicine, New Haven, USA. jinglan.wang@yale.edu.
Charles X MaUniversity of Connecticut School of Medicine, Farmington, USA. xiaodong88ma@gmail.com.
Xiao-Chun WangDepartment of Surgical Oncology, Affiliated Hospital of Hebei University, Baoding, China. xiaochun.wang@yale.edu.
Feng-Song LiuCollege of Life Sciences, Hebei University, Baoding, China. liufengsong@hbu.edu.cn.
Yale University · USAffiliated Hospital of Hebei University · CNHebei University · CNUniversity of Connecticut · US

Funding

THE JAZF1 AND 2 GENES IN UTERINE SARCOMASR01CA085995 · NCI · YALE UNIVERSITY · PI SKLAR, JEFFREY · 2000 to 2005
$1.5M
NCI NIH HHS CA-85995NCI NIH HHS R01 CA085995
6 · The paper itself

Abstract

backgroundThe metastasis-associated lung adenocarcinoma transcription 1 (Malat1) is a highly conserved long non-coding RNA (lncRNA) gene. Previous studies showed that Malat1 is abundantly expressed in many tissues and involves in promoting tumor growth and metastasis by modulating gene expression and target protein activities. However, little is known about the biological function and regulation mechanism of Malat1 in normal cell proliferation.

resultsIn this study we conformed that Malat1 is highly conserved across vast evolutionary distances amongst 20 species of mammals in terms of sequence, and found that mouse Malat1 expresses in tissues of liver, kidney, lung, heart, testis, spleen and brain, but not in skeletal muscle. After treating erythroid myeloid lymphoid (EML) cells with All-trans Retinoic Acid (ATRA), we investigated the expression and regulation of Malat1 during hematopoietic differentiation, the results showed that ATRA significantly down regulates Malat1 expression during the differentiation of EML cells. Mouse LRH (Lin-Rhodamine(low) Hoechst(low)) cells that represent the early-stage progenitor cells show a high level of Malat1 expression, while LRB (Lin - Hoechst(Low) Rhodamine(Bright)) cells that represent the late-stage progenitor cells had no detectable expression of Malat1. Knockdown experiment showed that depletion of Malat1 inhibits the EML cell proliferation. Along with the down regulation of Malat1, the tumor suppressor gene p53 was up regulated during the differentiation. Interestingly, we found two p53 binding motifs with help of bioinformatic tools, and the following chromatin immunoprecipitation (ChIP) test conformed that p53 acts as a transcription repressor that binds to Malat1's promoter. Furthermore, we testified that p53 over expression in EML cells causes down regulation of Malat1.

conclusionsIn summary, this study indicates Malat1 plays a critical role in maintaining the proliferation potential of early-stage hematopoietic cells. In addition to its biological function, the study also uncovers the regulation pattern of Malat1 expression mediated by p53 in hematopoietic differentiation. Our research shed a light on exploring the Malat1 biological role including therapeutic significance to inhibit the proliferation potential of malignant cells.

Indexed as

Cell DifferentiationEvolution, MolecularHematopoiesisAnimalsBone MarrowCell ProliferationConserved SequenceDown-RegulationHumansLiverLymphocytesMice, Inbred BALB CPrimatesPromoter Regions, GeneticProtein BindingRNA, Long NoncodingMALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseRNA, Long NoncodingTretinoinTumor Suppressor Protein p53

Identifiers

PMID26335021
PMCPMC4559210
OpenAlexW1912917036

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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.