Evidence map›Paper›PMID 31990345›Full record

ArticleJapanese journal of clinical oncology2020

Estrogen/estrogen receptor promotes the proliferation of endometrial carcinoma cells by enhancing hMOF expression.

Yue Qi, Mingzi Tan, Mingjun Zheng, Shan Jin, Huimin Wang, Juanjuan Liu, Peiyao Wang, Xin Nie, Lingling Gao, Bei Lin

Open access · hybridAbstract read
In one paragraph

Article in Japanese journal of clinical oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  10. Ferroptosis, Metabolic Rewiring, and Endometrial Cancer.International journal of molecular sciences · 2023
    Review
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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

10 authors at 2 institutions in 1 country.

Yue QiDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Mingzi TanDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Mingjun ZhengDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Shan JinDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Huimin WangDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Juanjuan LiuDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Peiyao WangDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Xin NieDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Lingling GaoDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
Bei LinDepartment of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang, Liaoning, China.
China Medical University · CNLiaoning Cancer Hospital & Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aims to analyse the expression of human MOF in endometrial carcinoma cells and its relationship with estrogen and estrogen receptor and to investigate the effect of estrogen-human MOF on the malignant biological behaviours of endometrial carcinoma cells.

methodsThe expression of human MOF was detected in different endometrial tissues by immunohistochemistry. The effects of human MOF, human MOF combined with estrogen stimulation and estrogen plus anti-human MOF antibody blocking on the proliferation of endometrial carcinoma cells were evaluated by western blotting, real-time polymerase chain reaction, cell proliferation assay and cell cycle distribution. Bioinformatics was used to identify the correlations of human MOF and estrogen and involved pathways.

resultsThe expression levels of human MOF in endometrial carcinoma tissues were significantly higher than that in atypical hyperplasia and normal endometrial tissues. High expression of human MOF was associated with late-stage cancer, lymph node metastasis and short survival time, and it was also an independent prognostic risk factor for endometrial carcinoma. After human MOF knockdown, the proliferation, migration and invasive capacity of Ishikawa cells decreased and cell apoptosis increased. After stimulation with estrogen, the PI3K/Akt and Ras-Raf-MEK-ERK signalling pathways were activated, and the expression of the human MOF protein was increased. human MOF (KAT8) expression showed a positive correlation with ESR1 expression, and KAT8-associated genes were enriched in the cell cycle pathways and splicing pathways.

conclusionHuman MOF was highly expressed in endometrial carcinoma and associated with proliferation. Estrogen/estrogen receptor enhanced human MOF expression; promoted the proliferation, migration and invasion of Ishikawa cells; and inhibited cell apoptosis by activating the PI3K/Akt and Ras-Raf-MEK-ERK signalling pathways.

Indexed as

AdultAgedApoptosisCell CycleCell Line, TumorCell ProliferationEndometrial NeoplasmsEndometriumEstrogensFemaleHistone AcetyltransferasesHumansMiddle AgedPhosphatidylinositol 3-KinasesProtein KinasesReceptors, EstrogenEstrogensHistone AcetyltransferasesKAT8 protein, humanPhosphatidylinositol 3-KinasesProtein KinasesReceptors, Estrogenendometrial carcinomaestrogenestrogen receptorhMOFproliferation

Identifiers

PMID31990345
PMCPMC7061248
OpenAlexW3004261171

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.