Evidence map›Paper›PMID 38281945›Full record

ArticleJournal of translational medicine2024

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Yan Li, Shenghan Lou, Jian Zhang, Shilu Zhao, Ge Lou

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

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  6. LncRNAs signatures in gynecological cancers: ovarian and endometrial cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

5 authors at 1 institution in 1 country.

Yan Li *Department of Obstetrics and Gynecology, First Affiliated Hospital of Harbin Medical University, Harbin, 150007, Heilongjiang, China.
Shenghan Lou *Department of Gynecology, Harbin Medical University Cancer Hospital, 150 HaPing Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Jian ZhangDepartment of Gynecology, Harbin Medical University Cancer Hospital, 150 HaPing Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Shilu ZhaoDepartment of Gynecology, Harbin Medical University Cancer Hospital, 150 HaPing Road, Nangang District, Harbin, 150081, Heilongjiang, China.
Ge LouDepartment of Gynecology, Harbin Medical University Cancer Hospital, 150 HaPing Road, Nangang District, Harbin, 150081, Heilongjiang, China. louge@ems.hrbmu.edu.cn.ORCID 0000-0001-6778-2340
Harbin Medical University · CN

Funding

First Affiliated Hospital of Harbin Medical University 2023M19National Natural Science Foundation of China 81872507National Natural Science Foundation of China 82173238Natural Science Foundation of Heilongjiang Province ZD2020H007
6 · The paper itself

Abstract

backgroundOvarian cancer poses a serious threat to women's health. Due to the difficulty of early detection, most patients are diagnosed with advanced-stage disease or peritoneal metastasis. We found that LncRNA MEG3 is a novel tumor suppressor, but its role in tumor occurrence and development is still unclear.

methodsWe investigated the expression level of MEG3 in pan-cancer through bioinformatics analysis, especially in gynecological tumors. Function assays were used to detect the effect of MEG3 on the malignant phenotype of ovarian cancer. RIP, RNA pull-down, MeRIP-qPCR, actinomycin D test were carried out to explore the m

resultsIn this study, we discovered that MEG3 was downregulated in various cancers, with the most apparent downregulation in ovarian cancer. MEG3 inhibited the proliferation, migration, and invasion of ovarian cancer cells. Overexpression of MEG3 suppressed the degradation of VASH1 by negatively regulating miR-885-5p, inhibiting the ovarian cancer malignant phenotype. Furthermore, we demonstrated that MEG3 was regulated at the posttranscriptional level. YTHDF2 facilitated MEG3 decay by recognizing METTL3‑mediated m

conclusionWe demonstrated that MEG3 is influenced by METTL3/YTHDF2 methylation and restrains ovarian cancer proliferation and metastasis by binding miR-885-5p to increase VASH1 expression. MEG3 is expected to become a therapeutic target for ovarian cancer.

Indexed as

MicroRNAsOvarian NeoplasmsRNA, Long NoncodingAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMethylationMethyltransferasesMiceCell Cycle ProteinsMEG3 non-coding RNA, humanMethyltransferasesMETTL3 protein, humanMicroRNAsMIRN885 microRNA, humanRNA, Long NoncodingVASH1 protein, humanm6A methylationMEG3Ovarian cancerVASH1

Identifiers

PMID38281945
PMCPMC10823642
OpenAlexW4391311730

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.