Evidence map›Paper›PMID 37124539›Full record

ArticleFrontiers in oncology2023

miR-1246 in tumor extracellular vesicles promotes metastasis

Masahiro Morimoto, Nako Maishi, Takuya Tsumita, Mohammad Towfik Alam, Hiroshi Kikuchi, Yasuhiro Hida, Yusuke Yoshioka, Takahiro Ochiya, Dorcas A Annan, Ryo Takeda and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Masahiro MorimotoDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Nako MaishiDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Takuya TsumitaDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Mohammad Towfik AlamDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Hiroshi KikuchiDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Yasuhiro HidaDepartment of Cardiovascular and Thoracic Surgery, Hokkaido University Faculty of Medicine, Sapporo, Japan.
Yusuke YoshiokaInstitute of Medical Science, Tokyo Medical University, Tokyo, Japan.
Takahiro OchiyaInstitute of Medical Science, Tokyo Medical University, Tokyo, Japan.
Dorcas A AnnanDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Ryo TakedaDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Yoshimasa KitagawaDepartment of Oral Diagnosis and Medicine, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Kyoko HidaDepartment of Vascular Biology and Molecular Pathology, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan.
Hokkaido University · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Tumor blood vessels play a key role in tumor metastasis. We have previously reported that tumor endothelial cells (TECs) exhibit abnormalities compared to normal endothelial cells. However, it is unclear how TECs acquire these abnormalities. Tumor cells secrete extracellular vesicles (EVs) to create a suitable environment for themselves. We have previously identified miR-1246 to be more abundant in high metastatic melanoma EVs than in low metastatic melanoma EVs. In the current study, we focused on miR-1246 as primarily responsible for acquiring abnormalities in TECs and examined whether the alteration of endothelial cell (EC) character by miR-1246 promotes cancer metastasis. Methods: We analyzed the effect of miR-1246 in metastatic melanoma, A375SM-EVs, Results: Intravenous administration of A375SM-EVs induced tumor cell colonization in the lung resulting in lung metastasis. In contrast, miR-1246 knockdown in A375SM decreased lung metastasis Conclusion: miR-1246 in high metastatic tumor EVs promotes lung metastasis by inducing the adhesion of tumor cells to ECs and destroying the EC barrier.

Indexed as

extracellular vesiclesICAM-1metastasismiRNAtumor endothelial cellVE-cadherin

Identifiers

PMID37124539
PMCPMC10130374
OpenAlexW4365148649

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.