Evidence map›Paper›PMID 28209128›Full record

ArticleBMC cancer2017

miR-296 inhibits the metastasis and epithelial-mesenchymal transition of colorectal cancer by targeting S100A4.

Zheng He, Lianhua Yu, Shiyi Luo, Mingzhen Li, Junbo Li, Qi Li, Yi Sun, Chengbin Wang

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  8. Polyploid giant cancer cells and cancer progression.Frontiers in cell and developmental biology · 2022
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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

8 authors at 5 institutions in 1 country.

Zheng HeDepartment of Clinical Laboratory, Chinese PLA General Hospital, No. 28 Fuxing Road, Beijing, 100853, China.
Lianhua YuDepartment of Laboratory Medicine, Taizhou Municipal Hospital, Taizhou, 318000, China.
Shiyi LuoState Key Laboratory of Physical Chemistry of Solid Surfaces and College of Chemistry and Chemical Engineering, Xiamen University, Xiamen, 361005, China.
Mingzhen LiBeijing Center for Physical and Chemical Analysis, Beijing, 100094, China.
Junbo LiBeijing Center for Physical and Chemical Analysis, Beijing, 100094, China.
Qi LiDepartment of Clinical Laboratory, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Yi SunDepartment of Clinical Laboratory, Chinese PLA General Hospital, No. 28 Fuxing Road, Beijing, 100853, China.
Chengbin WangDepartment of Clinical Laboratory, Chinese PLA General Hospital, No. 28 Fuxing Road, Beijing, 100853, China. wcb_pla@163.com.
Chinese PLA General Hospital · CNBeijing Academy of Science and Technology · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNTaizhou Municipal Hospital · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysregulation of microRNAs (miRNAs) is actively involved in the pathogenesis and tumorigenicity of colorectal cancer (CRC). miR-296 was found to play either oncogenic or tumor suppressive role in human cancers. However, the status of miR-296 and its function in CRC remain unknown.

methodsThe expression of miR-296 was confirmed by qRT-PCR in CRC tissues and cells, and its level was altered by corresponding miRNA vectors. Wound healing and Transwall assays were performed to detect the migration and invasion of CRC cells. The levels of proteins were measured using immunoblotting, immunohistochemistry and immunofluorescence.

resultsUnderexpression of miR-296 was disclosed in CRC tissues and cells. Its decreased level was evidently correlated with adverse clinical parameters and poor prognosis of CRC patients. In vitro experiments indicated that miR-296 inhibited CRC cell migration and invasion. Mechanically, miR-296 inhibited the epithelial-mesenchymal transition (EMT) of CRC cells. A negative correlation between miR-296 and S100A4 expression was observed in CRC tissues. Luciferase reporter assays indicated that miR-296 inversely regulated the luciferase activity of 3'-UTR of S100A4. Herein, S100A4 was found to be a downstream molecule of miR-296 in CRC. Furthermore, S100A4 mediated the anti-metastatic effects of miR-296 on EMT, migration and invasion of CRC cells.

conclusionsmiR-296 functions as an anti-metastatic factor mainly by suppressing S100A4 in CRC. It potentially acts as a prognostic predictor and a drug-target for CRC patients.

Indexed as

AdultAgedCell Line, TumorColonColorectal NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHistocytochemistryHumansMaleMicroRNAsMiddle AgedNeoplasm MetastasisReal-Time Polymerase Chain ReactionS100 Calcium-Binding Protein A4MicroRNAsMIRN296 microRNA, humanS100A4 protein, humanS100 Calcium-Binding Protein A4Colorectal cancerEpithelial-mesenchymal transitionMetastasismiR-296S100A4

Identifiers

PMID28209128
PMCPMC5311719
OpenAlexW2587809552

What OpenQuestion holds

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LicenceCC BY
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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.