Evidence map›Paper›PMID 38565081›Full record

ArticleNeuroendocrinology2024

Lysine Methyltransferase 5A Promotes the Progression of Growth Hormone Pituitary Neuroendocrine Tumors through the Wnt/β-Catenin Signaling Pathway.

Junjun Li, Hao Song, Ting Chen, Sixi Zhang, Chao Zhang, Chen Ma, Lingye Zhang, Tengfei Wang, Yuan Qian, Xingli Deng

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroendocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

10 authors at 4 institutions in 1 country.

Junjun LiDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Hao SongDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Ting ChenDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Sixi ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Chao ZhangXiangyang First People's Hospital, Xiangyang, China.
Chen MaDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Lingye ZhangDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Tengfei WangDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
Yuan QianThe Clinical Medical Research Center for Obstetrics and Gynecology (Yunnan Joint Key Laboratory), Kunming City of Maternal and Child Health Hospital, Kunming City of Women and Children Hospital, Kunming, China.
Xingli DengDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, China.
First Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CNTaiyuan Central Hospital · CNXiang Yang No.1 People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGrowth hormone (GH) secreting pituitary adenoma is considered one of the most harmful types of Pituitary Neuroendocrine Tumors (PitNETs). Our previous research has found that high expression of Lysine methyltransferase 5A (KMT5A) is closely related to the proliferation of PitNETs. The aim of this study was to investigate the role and molecular mechanism of KMT5A in the progression of GH PitNETs.

methodsImmunohistochemistry, qRT-PCR, and Western blot (WB) were used to assess the expression levels of KMT5A in human normal pituitary and GH PitNETs, as well as in rat normal pituitary and GH3 cells. Additionally, we utilized RNA interference technology and treatment with a selective KMT5A inhibitor to decrease the expression of KMT5A in GH3 cells. CCK-8, EdU, flow cytometry (FCM), clone formation, and WB assay were further employed to evaluate the impact of KMT5A on the proliferation of GH3 cells in vitro. A xenograft model was established to evaluate the role of KMT5A in GH PitNETs progression in vivo.

resultsKMT5A was highly expressed in GH PitNETs and GH3 cells. Moreover, the reduction of KMT5A expression led to inhibited growth of GH PitNETs and increased apoptosis of tumor cells, as indicated by the findings from CCK-8, EdU, clone formation, and FCM assays. Additionally, WB analysis identified the Wnt/β-catenin signaling pathway as a potential mechanism through which KMT5A promotes GH PitNETs progression.

conclusionOur research suggests that KMT5A may facilitate the progression of GH PitNETs via the Wnt/β-catenin signaling pathway. Therefore, KMT5A may serve as a potential therapeutic target and molecular biomarker for GH PitNETs.

Indexed as

Neuroendocrine TumorsWnt Signaling PathwayAdenomaAdultAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGrowth Hormone-Secreting Pituitary AdenomaHistone-Lysine N-MethyltransferaseHumansMaleMiceMice, NudeMiddle AgedHistone-Lysine N-MethyltransferaseKMT5A protein, humanGrowth hormoneKMT5APitNETsWnt/β-catenin

Identifiers

PMID38565081
PMCPMC11152009
OpenAlexW4393578765

What OpenQuestion holds

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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.