Evidence map›Paper›PMID 24632613›Full record

ArticleOncogene2015

miR-625 suppresses tumour migration and invasion by targeting IGF2BP1 in hepatocellular carcinoma.

X Zhou, C Z Zhang, S-X Lu, G G Chen, L-Z Li, L-L Liu, C Yi, J Fu, W Hu, J-M Wen and 1 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.9field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
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  12. Crucial Roles of miR-625 in Human Cancer.Frontiers in medicine · 2022
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  18. mFrontiers in oncology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

X Zhou1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China [3] Department of Pathology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
C Z Zhang1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
S-X Lu1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
G G ChenDepartment of Surgery, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
L-Z Li1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
L-L Liu1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
C Yi1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
J Fu1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
W Hu1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
J-M WenDepartment of Pathology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
J-P Yun1] Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China [2] Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, China.
State Key Laboratory of Oncology in South ChinaSun Yat-sen University · CNSun Yat-sen University Cancer Center · CNChinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most prevalent malignancies and the third leading cause of cancer-related deaths worldwide. Tumour metastasis is one of the major causes of high mortality. microRNAshave been implicated in HCC metastasis. In this study, we found that miR-625 was frequently downregulated in HCC samples. A decrease in miR-625 was significantly correlated with lymph node anddistance metastasis (P=0.013), the presence of portal venous invasion (P=0.036), tumor-node-metastasis (TNM) stage (P=0.027) and unfavourable overall survival (P=0.003). Compared with primary tumours, miR-625 expression was markedly reduced in portal venous metastatic tumours. Re-expression of miR-625 in HCC cells was remarkably effective in suppressing cell migration andinvasiveness in vitro and in vivo. Mechanistically, miR-625 was confirmed to downregulate IGF2 mRNA-binding protein 1(IGF2BP1) directly, the expression of which was inversely correlated with the level of miR-625 in HCC cell lines and tissues. High expression of IGF2BP1 was frequently found in HCC samples, and associated with poor prognosis. Knockdown of endogenous IGF2BP1 by siRNA exhibited similar effects as the overexpression of miR-625, whereas overexpression of IGF2BP1 (without the 3'-UTR) abrogated miR-625-mediated metastasis inhibition. Interference of the PTEN/HSP27 pathway contributed to miR-625-mediated metastasis inhibition. Taken together, our data suggest that miR-625 might function as an antimetastatic miRNA to have an important role in HCC progression by modulating the IGF2BP1/PTEN pathway. The newly identified miR-625/IGF2BP1 axis represents a new potential therapeutic target for HCC treatment.

Indexed as

AdultAgedAged, 80 and overAnimalsCarcinoma, HepatocellularCell MovementDown-RegulationFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHep G2 CellsHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CIGF2BP1 protein, humanMicroRNAsMIRN625 microRNA, humanRNA-Binding Proteins

Identifiers

PMID24632613
OpenAlexW2046382781

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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.