Evidence map›Paper›PMID 26617763›Full record

ArticleInternational journal of clinical and experimental pathology2015

Down-regualtion of miR-106b induces epithelial-mesenchymal transition but suppresses metastatic colonization by targeting Prrx1 in colorectal cancer.

Lin Zheng, Yuqin Zhang, Shuimiao Lin, Aimin Sun, Runze Chen, Yi Ding, Yanqing Ding

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  18. Regulatory miRNAs in Colorectal Carcinogenesis and Metastasis.International journal of molecular sciences · 2017
    Review
  19. Review
  20. MiR-106b promotes migration and invasion through enhancing EMT via downregulation of Smad 7 in Kazakh's esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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

7 authors at 2 institutions in 1 country.

Lin ZhengDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong Province, China ; Department of Pathology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Yuqin ZhangDepartment of Oncology, The First Affiliated Hospital of Jinan University Guangzhou 510630, Guangdong Province, China.
Shuimiao LinDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Aimin SunDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Runze ChenDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Yi DingDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Yanqing DingDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University Guangzhou 510515, Guangdong Province, China ; Department of Pathology, Nanfang Hospital, Southern Medical University Guangzhou 510515, Guangdong Province, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence identified that epithelial-mesenchymal transition (EMT) is acquired during progression to metastatic, but whether it is an absolute requirement is still controversial. MiR-106b has been confirmed to promote cancer cell proliferation; however few studies are available on its functions in EMT and metastasis in colorectal cancer (CRC). In this study, we found that knocking down miR-106b induced EMT conferring migratory and invasive properties. MiR-106b knockdown induced cytoskeletal reorganization through staining intracellular F-actin. The expression of Rho GTPases (Rac1 and Cdc42) and Tiam1 was significantly enforced after miR-106b down-regulation. However, miR-106b knocking down could suppress metastatic colonization in vivo. Correspondingly, over expression of miR-106b obtained an opposite effect. We identified Prrx1 was a direct target of miR-106b through using target prediction algorithms and dual-Luciferase reporter assay. Moreover, Moreover, we also found TGF-β1 could down-regulate miR-106b, and simultaneously miR-106b also influences the expression of TGF-β1, establishing a negative feedback loop to regulate the expression of Prrx1 together. Taken together, these findings demonstrated that miR-106b knockdown could induce EMT which conferring cells migratory and invasive properties but could not accomplish distant metastatic colonization efficiently.

Indexed as

Blotting, WesternCell MovementColorectal NeoplasmsDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGene Knockdown TechniquesHomeodomain ProteinsHumansMicroRNAsNeoplasm InvasivenessPolymerase Chain ReactionRNA, Small InterferingTransfectionHomeodomain ProteinsMicroRNAsMIRN106 microRNA, humanPRRX1 protein, humanRNA, Small Interferingcolorectal cancerEMTmetastasismiR-106bPrrx1

Identifiers

PMID26617763
PMCPMC4637578
OpenAlexW2185304108

What OpenQuestion holds

Textmetadata
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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.