Evidence map›Paper›PMID 25693145›Full record

ArticlePLoS genetics2015

Systemic delivery of microRNA-101 potently inhibits hepatocellular carcinoma in vivo by repressing multiple targets.

Fang Zheng, Yi-Ji Liao, Mu-Yan Cai, Tian-Hao Liu, Shu-Peng Chen, Pei-Hong Wu, Long Wu, Xiu-Wu Bian, Xin-Yuan Guan, Yi-Xin Zeng and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS genetics, 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 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

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

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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 2 countries.

Fang ZhengThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Medical Research Center, Sun Yat-Sen Memorial Hospital, Guangzhou, China.
Yi-Ji LiaoThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Mu-Yan CaiThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Tian-Hao LiuThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Medical Research Center, Sun Yat-Sen Memorial Hospital, Guangzhou, China.
Shu-Peng ChenThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Pei-Hong WuThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Tumor Interventional Therapy, Sun Yat-Sen University Cancer Center, Guangzhou, China; Hepatobiliary Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Long WuDepartment of Clinical Oncology, People's Hospital, Wuhan University, Wuhan, China.
Xiu-Wu BianInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xin-Yuan GuanThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Department of Clinical Oncology, the University of Hong Kong, Hong Kong, China.
Yi-Xin ZengThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Yun-Fei YuanThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Hepatobiliary Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Hsiang-Fu KungThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; State Key Laboratory of Oncology in South China, the Chinese University of Hong Kong, Hong Kong, China.
Dan XieThe State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNChinese University of Hong Kong · CNSouthwest Hospital · CNSun Yat-sen Memorial Hospital · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted therapy based on adjustment of microRNA (miRNA)s activity takes great promise due to the ability of these small RNAs to modulate cellular behavior. However, the efficacy of miR-101 replacement therapy to hepatocellular carcinoma (HCC) remains unclear. In the current study, we first observed that plasma levels of miR-101 were significantly lower in distant metastatic HCC patients than in HCCs without distant metastasis, and down-regulation of plasma miR-101 predicted a worse disease-free survival (DFS, P<0.05). In an animal model of HCC, we demonstrated that systemic delivery of lentivirus-mediated miR-101 abrogated HCC growth in the liver, intrahepatic metastasis and distant metastasis to the lung and to the mediastinum, resulting in a dramatic suppression of HCC development and metastasis in mice without toxicity and extending life expectancy. Furthermore, enforced overexpression of miR-101 in HCC cells not only decreased EZH2, COX2 and STMN1, but also directly down-regulated a novel target ROCK2, inhibited Rho/Rac GTPase activation, and blocked HCC cells epithelial-mesenchymal transition (EMT) and angiogenesis, inducing a strong abrogation of HCC tumorigenesis and aggressiveness both in vitro and in vivo. These results provide proof-of-concept support for systemic delivery of lentivirus-mediated miR-101 as a powerful anti-HCC therapeutic modality by repressing multiple molecular targets.

Indexed as

Molecular Targeted TherapyAdultAnimalsCarcinogenesisCarcinoma, HepatocellularCell Line, TumorDisease-Free SurvivalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMicroRNAsMiddle AgedMicroRNAsMIRN101 microRNA, humanrho-Associated KinasesROCK2 protein, human

Identifiers

PMID25693145
PMCPMC4334495
OpenAlexW2034402063

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.