Evidence map›Paper›PMID 33472171›Full record

ArticleAging2020

Functional characterization of DLK1/MEG3 locus on chromosome 14q32.2 reveals the differentiation of pituitary neuroendocrine tumors.

Yiyuan Chen, Hua Gao, Qian Liu, Weiyan Xie, Bin Li, Sen Cheng, Jing Guo, Qiuyue Fang, Haibo Zhu, Zhuang Wang and 3 more

Abstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

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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

5 citing papers in PubMed.

  1. Article
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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

13 authors.

Yiyuan ChenDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Hua GaoDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Qian LiuDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Weiyan XieDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Bin LiDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Sen ChengDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Jing GuoDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Qiuyue FangDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Haibo ZhuDepartment of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China.
Zhuang WangDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Jichao WangDepartment of Neurosurgery, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang 830001, China.
Chuzhong LiDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.
Yazhuo ZhangDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pituitary neuroendocrine tumors (PitNETs) represent the neoplastic proliferation of the anterior pituitary gland. Transcription factors play a key role in the differentiation of PitNETs. However, for a substantial proportion of PitNETs, the etiology is poorly understood. According to the transcription data of 172 patients, we found the imprinting disorders of the 14q32.2 region and DLK1/MEG3 locus associated with the differentiation of PitNETs. DLK1/MEG3 locus promoted somatotroph differentiation and inhibited tumor proliferation in PIT1(+) patients, furthermore, the level of DLK1 played a critical role in the trend of somatotroph or lactotroph differentiation. Anti-DLK1 monoclonal antibody blockade or siMEG3 both indicated that the DLK1/MEG3 significantly promoted the synthesis and secretion of GH/IGF-1 and inhibited cell proliferation. In addition, loss of DLK1 activated the mTOR signaling pathway in high DLK1-expressing and PIT1(+) GH3 cell lines, a mild effect in the low DLK1-expressing and PIT1(+) MMQ cell lines and no effect in the PIT1(-) ATT20 cell line. These findings emphasize that expression at the DLK1/MEG3 locus plays a key role in the differentiation of PitNETs, especially somatotroph adenomas, and provide potential molecular target data for patient stratification and treatment in the future.

Indexed as

ACTH-Secreting Pituitary AdenomaAdenomaAdultAgedAnimalsCalcium-Binding ProteinsCell DifferentiationCell Line, TumorCell ProliferationFemaleGene Expression ProfilingGenomic ImprintingGonadotropins, PituitaryGrowth HormoneGrowth Hormone-Secreting Pituitary AdenomaHumansCalcium-Binding ProteinsDLK1 protein, humanDlk1 protein, mouseDlk1 protein, ratGonadotropins, PituitaryGrowth HormoneInsulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsMEG3 non-coding RNA, humanMEG3 non-coding RNA, mouseMEG3 non-coding RNA, ratMembrane ProteinsRNA, Long NoncodingTOR Serine-Threonine KinasesdifferentiationDLK1/MEG3 locusgrowth hormone secretingpituitary neuroendocrine tumorssomatotroph adenomas

Identifiers

PMID33472171
PMCPMC7835058

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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.