Evidence map›Paper›PMID 26284494›Full record

ArticleMolecular and cellular endocrinology2015

Tumor suppression by MEG3 lncRNA in a human pituitary tumor derived cell line.

Paweena Chunharojrith, Yuki Nakayama, Xiaobing Jiang, Rachel E Kery, Jun Ma, Cristine S De La Hoz Ulloa, Xun Zhang, Yunli Zhou, Anne Klibanski

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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  6. Noncoding RNAs: biology and applications-a Keystone Symposia report.Annals of the New York Academy of Sciences · 2021
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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

9 authors at 1 institution in 1 country.

Paweena ChunharojrithNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Yuki NakayamaNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Xiaobing JiangNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Rachel E KeryNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Jun MaNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Cristine S De La Hoz UlloaNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Xun ZhangNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Yunli ZhouNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: yunli.zhou@mgh.harvard.edu.
Anne KlibanskiNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Harvard University · US

Funding

HORMONE REGULATION AND PATHOGENESIS OF PITUITARY TUMORSR01DK040947 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI KLIBANSKI, ANNE · 1989 to 2010
$2.7M
NIDDK NIH HHS R01 DK040947NIDDK NIH HHS R01DK40947
6 · The paper itself

Abstract

Human clinically non-functioning pituitary adenomas (NFAs) account for approximately 40% of diagnosed pituitary tumors. Epigenetic mutations in tumor suppressive genes play an important role in NFA development. Maternally expressed gene 3 (MEG3) is a long non-coding RNA (lncRNA) and we hypothesized that it is a candidate tumor suppressor whose epigenetic silencing is specifically linked to NFA development. In this study, we introduced MEG3 expression into PDFS cells, derived from a human NFA, using both inducible and constitutively active expression systems. MEG3 expression significantly suppressed xenograft tumor growth in vivo in nude mice. When induced in culture, MEG3 caused cell cycle arrest at the G1 phase. In addition, inactivation of p53 completely abolished tumor suppression by MEG3, indicating that MEG3 tumor suppression is mediated by p53. In conclusion, our data support the hypothesis that MEG3 is a lncRNA tumor suppressor in the pituitary and its inactivation contributes to NFA development.

Indexed as

Genes, Tumor SuppressorAcetylationAnimalsCell Cycle CheckpointsCell Line, TumorEpigenesis, GeneticFemaleG1 PhaseHeterograftsHumansMiceMice, NudePituitary GlandPituitary NeoplasmsPrimary Cell CultureRNA, Long NoncodingMEG3 non-coding RNA, humanRNA, Long NoncodingTumor Suppressor Protein p53Long non-coding RNAMEG3p53Pituitary tumorTumor suppression

Identifiers

PMID26284494
PMCPMC4605874
OpenAlexW1191344064

What OpenQuestion holds

Textmetadata
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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.