Evidence map›Paper›PMID 36281372›Full record

ArticleHeliyon2022

MiR-23b-3p suppresses epithelial-mesenchymal transition, migration, and invasion of hepatocellular carcinoma cells by targeting c-MET.

Na Ri Park, Jung Hoon Cha, Pil Soo Sung, Jeong Won Jang, Jong Young Choi, Seung Kew Yoon, Si Hyun Bae

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

Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  4. Core microRNAs regulate neural crest delamination and condensation in the developing trigeminal ganglion.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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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

7 authors at 2 institutions in 1 country.

Na Ri ParkThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Jung Hoon ChaThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Pil Soo SungThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Jeong Won JangThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Jong Young ChoiThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Seung Kew YoonThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
Si Hyun BaeThe Catholic University Liver Research Center, College of Medicine, The Catholic University of Korea, Seoul, 06591, Republic of Korea.
The Catholic University of Korea Seoul St. Mary's Hospital · KRCatholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Aberrant expression of c-MET is known to be associated with tumor recurrence and metastasis by promoting cell proliferation, epithelial-mesenchymal transition (EMT), and migration in hepatocellular carcinoma (HCC). Recently, miR-23b-3p has been identified as a tumor suppressor, but detailed role of miR-23b-3p in HCC is still unclear. Our study aimed to investigate how miR-23b-3p is associated with the malignant potential of HCC cells. Methods: HCC tissues and their adjacent non-tumor tissues were acquired from 30 patients with HCC. Expression of EMT- or stemness-related genes were examined in the two HCC cell lines. Migration of HCC cells was analyzed using transwell and wound healing assays. Results: c-MET was overexpressed in HCC tissues compared to the adjacent non-tumor tissues. c-MET knockdown inhibited EMT and reduced migration and invasion of HCC cells. Furthermore, c-MET was a target of miR-23b-3p, and miR-23b-3p expression was decreased in HCC tissues compared to non-tumor tissues. Treatment of miR-23b-3p inhibitor in HCC cells promoted EMT, cell migration, and invasion. In contrast, miR-23b-3p overexpression suppressed EMT, cell migration, and invasion, concomitantly reducing c-MET expression. Transfection of miR-23b-3p inhibitor with concomitant c-MET knockdown mitigated the effects of miR-23b-3p inhibitor on EMT in HCC cells. In addition, transforming growth factor beta1 (TGF-β1) stimulation after miR-23b-3p overexpression induced neither the mesenchymal phenotype nor migratory property of HCC cells. Conclusion: In this study, we confirmed that miR-23b-3p downregulation significantly increased EMT, migration, and invasion of HCC cells. In addition, c-MET was confirmed to be a target of miR-23b-3p in HCC cells and regulated the functional effects of miR-23b-3p. These results suggest that miR-23b-3p can be used as a prognostic biomarker and candidate target for HCC treatment.

Indexed as

c-METEpithelial-mesenchymal transition (EMT)Hepatocellular carcinoma (HCC)miR-23b-3pTransforming growth factor beta1 (TGF-β1)

Identifiers

PMID36281372
PMCPMC9586913
OpenAlexW4306377731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.