Evidence map›Paper›PMID 31796150›Full record

ArticleOncology research2020

MicroRNA-6884-5p Regulates the Proliferation, Invasion, and EMT of Gastric Cancer Cells by Directly Targeting S100A16.

Huifang Lv, Honglin Hou, Huijun Lei, Caiyun Nie, Beibei Chen, Liangyu Bie, Lili Han, Xiaobing Chen

Abstract read
In one paragraph

Article in Oncology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

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  20. Journal of Cancer · 2020
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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.

Huifang LvDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Honglin HouDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Huijun LeiDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Caiyun NieDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Beibei ChenDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Liangyu BieDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Lili HanDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.
Xiaobing ChenDepartment of Oncology, The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer HospitalZhengzhouChina.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

S100 binding protein A16 (S100A16) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of S100A16 are reported during the progression of many cancers. Our study mainly explored the interaction between S100A16 and miR-6884-5p in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the level of S100A16 and miR-6884-5p in GC tissues and cell lines. The si-S100A16, pcDNA-S100A16, miR-6884-5p mimic or inhibitor was transfected into GC cells, and the effects of S100A16 and miR-6884-5p on the proliferation, invasion, and epithelial-mesenchymal transition (EMT) were explored by qRT-PCR and Western blot assays. Luciferase assays were performed to validate S100A16 as an miR-6884-5p target in GC cells. In our study, we found that the level of miR-6884-5p was significantly decreased and the expression of S100A16 was significantly increased in GC tissues and cell lines. There was a close association between these changes. Knockdown of S100A16 significantly inhibited the proliferation, invasion, and EMT of GC cells. The bioinformatics analysis predicted that S100A16 is a potential target gene of miR-6884-5p, and the luciferase reporter assay confirmed that miR-6884-5p could directly target S100A16. Introduction of miR-6884-5p to GC cells had similar effects to S100A16 silencing. Overexpression of S100A16 in GC cells partially reversed the inhibitory effects of the miR-6884-5p mimic. miR-6884-5p inhibited the proliferation, invasion, and EMT of GC cells by directly decreasing S100A16 expression.

Indexed as

Gene Expression Regulation, NeoplasticRNA InterferenceBiomarkersCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Knockdown TechniquesHumansMatrix Metalloproteinase 2Matrix Metalloproteinase 9MicroRNAsS100 ProteinsStomach NeoplasmsTissue Inhibitor of Metalloproteinase-1BiomarkersMatrix Metalloproteinase 2Matrix Metalloproteinase 9MicroRNAsMMP2 protein, humanMMP9 protein, humanS100A16 protein, humanS100 ProteinsTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID31796150
PMCPMC7851531

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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.