Evidence map›Paper›PMID 27244080›Full record

ArticleScientific reports2016

miR-139-5p Inhibits the Epithelial-Mesenchymal Transition and Enhances the Chemotherapeutic Sensitivity of Colorectal Cancer Cells by Downregulating BCL2.

Qingguo Li, Xin Liang, Yuwei Wang, Xianke Meng, Ye Xu, Sanjun Cai, Zhimin Wang, Jianwen Liu, Guoxiang Cai

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

71 citing papers in PubMed, 1 synthesis or guideline pooled it.

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

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

9 authors.

Qingguo LiDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Xin LiangState Key Laboratory of Bioreactor Engineering &Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China.
Yuwei WangDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Xianke MengDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Ye XuDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Sanjun CaiDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Zhimin WangDepartment of Genetics, Shanghai-MOST Key Laboratory of Health and Disease Genomics, Chinese National Human Genome Center and Shanghai Academy of Science &Technology, Shanghai 201203, China.
Jianwen LiuState Key Laboratory of Bioreactor Engineering &Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China.
Guoxiang CaiDepartment of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are important regulators involved in various cancers, including colorectal cancer (CRC). The functions and mechanisms of the miRNAs involved in CRC progress and metastasis are largely unknown. In this study, miRNA microarray analysis was performed to screen crucial miRNAs involved in CRC progress, and miR-139-5p was chosen for further study. The functional roles of miR-139-5p in colon cancer were demonstrated by CCK-8 proliferation assay, cell invasion and migration, cell apoptosis and in a KO mouse study. miR-139-5p expression was significantly decreased in cancer tissues compared to normal tissues. The miR-139-5p expression level was associated with tumour stage (P < 0.01). Function studies revealed that miR-139-5p was significantly correlated with the metastasis potential and drug resistance of colon cancer cells by affecting the epithelial-mesenchymal transition (EMT). Then, we identified BCL2 as a direct target of miR-139-5p cells in vitro. The patient samples and KO mice model showed that BCL2 expression was inversely correlated with the expression of miR-139-5p. In conclusion, we found that miR-139-5p targeted the BCL2 pathway to reduce tumour metastasis and drug sensitivity in CRC. This axis provided insight into the mechanism underlying miRNA regulation of CRC metastasis and a novel therapeutic target for CRC therapy.

Indexed as

Drug Resistance, Neoplasm3' Untranslated RegionsAnimalsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansMiceMicroRNAsNeoplasm Transplantation3' Untranslated RegionsBCL2 protein, humanMicroRNAsMIRN139 microRNA, humanProto-Oncogene Proteins c-bcl-2

Identifiers

PMID27244080
PMCPMC4886683

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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.