Evidence map›Paper›PMID 39062818›Full record

ArticleInternational journal of molecular sciences2024

MEG3-Mediated Oral Squamous-Cell-Carcinoma-Derived Exosomal miR-421 Activates Angiogenesis by Targeting HS2ST1 in Vascular Endothelial Cells.

Chia-Yun Huang, Sung-Tau Chou, Yuan-Ming Hsu, Wan-Ju Chao, Guan-Hsun Wu, Jenn-Ren Hsiao, Horng-Dar Wang, Shine-Gwo Shiah

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

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

13 citing papers in PubMed.

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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

8 authors.

Chia-Yun HuangNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.
Sung-Tau ChouNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.
Yuan-Ming HsuNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.
Wan-Ju ChaoNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.
Guan-Hsun WuNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.
Jenn-Ren HsiaoHead and Neck Collaborative Oncology Group, Department of Otolaryngology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 704302, Taiwan.
Horng-Dar WangInstitute of Biotechnology, National Tsing Hua University, Hsinchu 300044, Taiwan.ORCID 0000-0001-9570-3611
Shine-Gwo ShiahNational Institute of Cancer Research, National Health Research Institutes, Miaoli 350401, Taiwan.ORCID 0000-0002-1003-973X

Funding

Ministry of Health and Welfare, Taiwan MOHW112-TDU-B-222-124012Ministry of Health and Welfare, Taiwan MOHW112-TDU-B-222-124014Ministry of Science and Technology, Taiwan MOST-111-2314-B-400-037-National Health Research Institutes, Taiwan NHRI-CA-111-PP03National Health Research Institutes, Taiwan NHRI-CA-112-PP03
6 · The paper itself

Abstract

Exosomal microRNAs (miRNAs) from cancer cells play a key role in mediating the oral squamous cell carcinoma (OSCC) microenvironment. The objective of this study was to investigate how the long non-coding RNA (lncRNA) MEG3 affects OSCC angiogenesis through exosomal miR-421. Global miRNA microarray analysis and quantitative real-time PCR (qRT-PCR) were performed to determine the level of miRNAs in OSCC cell-derived exosomes. Cell migration, invasion, tube formation, immunohistochemistry, and hemoglobin concentrations were used to study the effects of exosomal miR-421 in angiogenesis. Western blotting was used to determine the expression level of HS2ST1 and VEGFR2-related downstream proteins. MiRNA array and qRT-PCR identified the upregulation of miR-421 in OSCC cell-derived exosomes. Furthermore, exosomal miR-421 can be taken up by human umbilical vein endothelial cells (HUVECs) and then target HS2ST1 through VEGF-mediated ERK and AKT phosphorylation, thereby promoting HUVEC migration, invasion, and tube formation. Additionally, forced expression of the lncRNA MEG3 in OSCC cells reduced exosomal miR-421 levels and then increased HS2ST1 expression, thereby reducing the VEGF/VEGFR2 pathway in HUVECs. Our results demonstrate a novel mechanism by which lncRNA MEG3 can act as a tumor suppressor and regulate endothelial angiogenesis through the exosomal miR-421/HS2ST1 axis, which provides a potential therapeutic strategy for OSCC angiogenesis.

Indexed as

Carcinoma, Squamous CellCell MovementExosomesGene Expression Regulation, NeoplasticHuman Umbilical Vein Endothelial CellsMicroRNAsMouth NeoplasmsNeovascularization, PathologicRNA, Long NoncodingAngiogenesisCell Line, TumorHumansVascular Endothelial Growth Factor Receptor-2MEG3 non-coding RNA, humanMicroRNAsMIRN421 microRNA, humanRNA, Long NoncodingVascular Endothelial Growth Factor Receptor-2angiogenesisexosomeHS2ST1long non-coding RNA (lncRNA)microRNAmiR-421oral squamous cell carcinoma (OSCC)

Identifiers

PMID39062818
PMCPMC11277508

What Socratic 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 Socratic graph.