Evidence map›Paper›PMID 33571679›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021

Tumor-derived exosomal microRNA-106b-5p activates EMT-cancer cell and M2-subtype TAM interaction to facilitate CRC metastasis.

Chaogang Yang, Rongzhang Dou, Chen Wei, Keshu Liu, Dongdong Shi, Chunxiao Zhang, Qing Liu, Shuyi Wang, Bin Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
11.4field-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

140 citing papers in PubMed, 199 citations in OpenAlex.

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80 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 at 2 institutions in 1 country.

Chaogang YangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China; The Clinical Medical Research Center of Peritoneal Cancer of Wuhan, Wuhan 430071, China.
Rongzhang DouDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China.
Chen WeiDepartment of Internal Medicine, Affiliated Tumor Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China.
Keshu LiuDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China.
Dongdong ShiDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China; The Clinical Medical Research Center of Peritoneal Cancer of Wuhan, Wuhan 430071, China.
Chunxiao ZhangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China; The Clinical Medical Research Center of Peritoneal Cancer of Wuhan, Wuhan 430071, China.
Qing LiuDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China.
Shuyi WangDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China; The Clinical Medical Research Center of Peritoneal Cancer of Wuhan, Wuhan 430071, China. Electronic address: shuyiwang@whu.edu.cn.
Bin XiongDepartment of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China; Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, China; Hubei Cancer Clinical Study Center, Wuhan 430071, China; The Clinical Medical Research Center of Peritoneal Cancer of Wuhan, Wuhan 430071, China. Electronic address: binxiong1961@whu.edu.cn.
Wuhan University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is reported to involve in the crosstalk between tumor cells and tumor-associated macrophages (TAMs). Exosomes are considered as important mediators of orchestrating intercellular communication. However, the underlying mechanisms by which EMT-colorectal cancer (CRC) cells promote the M2 polarization of TAMs remain less understood. In this study, we found that EMT-CRC cells promoted the M2-like polarization of macrophages by directly transferring exosomes to macrophages, leading to a significant increase of the microRNA-106b-5p (miR-106b) level in macrophages. Mechanically, an increased level of miR-106b activated the phosphatidylinositol 3-kinase (PI3K)γ/AKT/mammalian target of rapamycin (mTOR) signaling cascade by directly suppressing programmed cell death 4 (PDCD4) in a post-transcription level, contributing to the M2 polarization of macrophages. Activated M2 macrophages, in a positive-feedback manner, promote EMT-mediated migration, invasion, and metastasis of CRC cells. Clinically, miR-106b was significantly elevated in CRC tissues and negatively correlated with the levels of PDCD4 in CRC specimens, and high expression of exosomal miR-106b in plasma was significantly associated with the malignant progression of CRC. Taken together, our results indicate that exosomal miR-106b derived from EMT-CRC cells has an important role in intercellular communication for inducing M2 macrophage polarization, illuminating a novel mechanism underlying CRC progression and offering potential targets for prevention of CRC metastasis.

Indexed as

BiomarkersCell Line, TumorCell MovementColorectal NeoplasmsEpithelial-Mesenchymal TransitionExosomesGene Expression Regulation, NeoplasticHumansMacrophage ActivationMacrophagesMicroRNAsModels, BiologicalNeoplasm MetastasisNeoplasm StagingPhosphatidylinositol 3-KinasesSignal TransductionBiomarkersMicroRNAsMIRN106 microRNA, humanPhosphatidylinositol 3-KinasesTOR Serine-Threonine Kinasescolorectal cancerEMTexosomemacrophagesmiR-106bPDCD4

Identifiers

PMID33571679
PMCPMC8178444
OpenAlexW3128874927

What OpenQuestion holds

Textmetadata
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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.