Evidence map›Paper›PMID 27673564›Full record

ArticleMolecular therapy. Nucleic acids2016

miR-181a Induces Macrophage Polarized to M2 Phenotype and Promotes M2 Macrophage-mediated Tumor Cell Metastasis by Targeting KLF6 and C/EBPα.

Jia Bi, Xianxin Zeng, Lin Zhao, Qian Wei, Lifeng Yu, Xinnan Wang, Zhaojin Yu, Yaming Cao, Fengping Shan, Minjie Wei

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular therapy. Nucleic acids, 2016. 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 It has been retracted, and should not be counted.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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. MicroRNAs in Macrophages: Regulators of Activation and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Jia BiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Xianxin ZengDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Lin ZhaoDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Qian WeiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Lifeng YuDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Xinnan WangDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Zhaojin YuDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
Yaming CaoDepartment of Immunology, School of Basic Medical Science, China Medical university, Shenyang, Liaoning, China.
Fengping ShanDepartment of Immunology, School of Basic Medical Science, China Medical university, Shenyang, Liaoning, China.
Minjie WeiDepartment of Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning, China.
China Medical University · CN

Funding

HSRD VA RCS 14-232
6 · The paper itself

Abstract

Macrophages can acquire a variety of polarization status and functions: classically activated macrophages (M1 macrophages); alternatively activated macrophages (M2 macrophages). However, the molecular basis of the process is still unclear. Here, this study addresses that microRNA-181a (miR-181a) is a key molecule controlling macrophage polarization. We found that miR-181a is overexpressed in M2 macrophages than in M1 macrophages. miR-181a expression was decreased when M2 phenotype converted to M1, whereas it increased when M1 phenotype converted to M2. Overexpression of miR-181a in M1 macrophages diminished M1 phenotype expression while promoting polarization to the M2 phenotype. In contrast, knockdown of miR-181a in M2 macrophages promoted M1 polarization and diminished M2 phenotype expression. Mechanistically, Bioinformatic analysis revealed that Kruppel-like factor 6 (KLF6) and CCAAT/enhancer binding protein-α (C/EBPα) is a potential target of miR-181a and luciferase assay confirmed that KLF6 and C/EBPα translation is suppressed by miR-181a through interaction with the 3'UTR of KLF6 and C/EBPα mRNA. Further analysis showed that induction of miR-181a suppressed KLF6 and C/EBPα protein expression. Importantly, miR-181a also diminishes M2 macrophages-mediated migration and invasion capacity of tumor cells. Collectively, our results suggest that miR-181a plays a significant role in regulating macrophage polarization through directly target KLF6 and C/EBPα.

Identifiers

PMID27673564
PMCPMC5056994
OpenAlexW2526085451

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.