Evidence map›Paper›PMID 29530052›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Exosomal microRNA-32-5p induces multidrug resistance in hepatocellular carcinoma via the PI3K/Akt pathway.

Xiao Fu, Mengjie Liu, Shengyang Qu, Jiequn Ma, Yamin Zhang, Tingting Shi, Hongqing Wen, Yujuan Yang, Shuhong Wang, Jing Wang and 3 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

149 citing papers in PubMed, 219 citations in OpenAlex.

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89 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 2 institutions in 1 country.

Xiao FuDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Mengjie LiuDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Shengyang QuDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Jiequn MaDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Yamin ZhangDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Tingting ShiDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Hongqing WenDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Yujuan YangThe Third Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi province, 710068, People's Republic of China.
Shuhong WangDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Jing WangDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Kejun NanDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China.
Yu YaoDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China. 13572101611@163.com.
Tao TianDepartment of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 Yanta West Road, Xi'an, Shaanxi, 710061, People's Republic of China. tiantao0607@163.com.
First Affiliated Hospital of Xi'an Jiaotong University · CNShaanxi Provincial People's Hospital · CN

Funding

International Cooperation Project in Science and Technology of Shaanxi Province 2016KW-017National Natural Science Foundation of China 81301909National Natural Science Foundation of China 81672810National Science Foundation of Shaanxi Province 2017JM8019
6 · The paper itself

Abstract

backgroundMultidrug resistance is the main obstacle for hepatocellular carcinoma (HCC) treatment. miR-32-5p is involved in HCC progression but its function in multidrug resistance is still unclear. Here we aim to find out the function of miR-32-5p in inducing multidrug resistance and its underlying mechanisms of transforming sensitive cell to resistant cell.

methodsWe detected the expression of miR-32-5p and PTEN in the multidrug-resistant cell line (Bel/5-FU) and the sensitive cell line (Bel7402), HCC and para-carcinoma liver tissues through real-time PCR. Dual-luciferase reporter assay verified PTEN is the target of miR-32-5p. Exosomes from sensitive and multidrug resistant cell line were obtained and confirmed through ultracentrifuge and Nano Analyzer. Gain- and loss-of-function experiments, rescue experiments, a PI3K/Akt pathway inhibitor, an exosome biogenesis inhibitor, and nude mice xenograft models were used to determine the underlying mechanisms of miR-32-5p and PTEN, as well as exosomal miR-32-5p in inducing multidrug resistance in vitro and in vivo.

resultsmiR-32-5p was significantly elevated but PTEN was reduced in Bel/5-FU. An inverse correlation between miR-32-5p and PTEN was confirmed in HCC cell lines and patients; moreover, high expression of miR-32-5p and low expression of PTEN were positively associated with poor prognosis. Over-expression of miR-32-5p activated the PI3K/Akt pathway by suppressing PTEN and induced multidrug resistance via exosomes through promoting angiogenesis and epithelial-mesenchymal transition (EMT).

conclusionsOur study demonstrated that the multidrug-resistant cell, Bel/5-FU delivers miR-32-5p to sensitive cell, Bel7402 by exosomes and activates the PI3K/Akt pathway to further induce multidrug resistance by modulating angiogenesis and EMT.

Indexed as

3' Untranslated RegionsAdultAgedAnimalsApoptosisBiological TransportCarcinoma, HepatocellularCell Line, TumorDisease Models, AnimalDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionExosomesFemaleGene Expression Regulation, NeoplasticGenes, ReporterHumans3' Untranslated RegionsMicroRNAsMIRN32 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseExosomeHepatocellular carcinomamicroRNA-32-5pMultidrug resistancePTEN

Identifiers

PMID29530052
PMCPMC5846230
OpenAlexW2807180358

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.