Evidence map›Paper›PMID 27142596›Full record

ArticleClinical & experimental metastasis2016

MicroRNA-106a functions as an oncogene in human gastric cancer and contributes to proliferation and metastasis in vitro and in vivo.

Meng Zhu, Ning Zhang, Shuixiang He, Ruirui Yan, Jun Zhang

Abstract read
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In one paragraph

Article in Clinical & experimental metastasis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Meng ZhuDepartment of Gastroenterology, General Hospital of Ningxia Medical University, 804 Shengli Street, Yinchuan, 750004, Ningxia, People's Republic of China.
Ning ZhangDepartment of Pathology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, People's Republic of China.
Shuixiang HeDepartment of Gastroenterology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China. hesx123@126.com.
Ruirui YanDepartment of Infectious Diseases, The Eighth Hospital of Xi'an, Xi'an, Shaanxi, People's Republic of China.
Jun ZhangDepartment of Gastroenterology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, People's Republic of China.
First Affiliated Hospital of Xi'an Jiaotong University · CNNingxia Medical University · CNThe Eighth Hospital of Xi'an · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidences has shown that miRNAs are involved in the development and progression of gastric cancer acts as tumor suppressor genes or oncogenes. In our previous studies, we have found that the up-regulation of miR-106a occurs frequently in human gastric cancer tissues compared with that of normal tissues. Here, we investigate the role of the ectopic expressed miR-106a in the progression and metastasis of gastric cancer in vitro and in vivo. FFPE samples have the priority to be included and qRT-PCR was used to detect the miR-106a expression. Human gastric cancer cells and immortalized gastric epithelial cell were selected and the miR-106a mimic and inhibitor were transfected. Cell growth was determined by MTT method. The flow cytometric analysis for cell apoptosis and transwell assays for evaluating the cell migration and invasion were conducted. Luciferase assay and western blot confirmed the direct binding site of miR-106a and its target. BALB/c nude mice were randomly divided to explore the implantation of gastric cancer cells transfected with miR-106a antagomir. Abnormal over-expression of miR-106a significantly promoted gastric cancer cell proliferation, metastasis, inhibited the cell apoptosis. Functional experiment ascertained that miR-106a interacted with FAS and mediated caspase3 pathway. Knockdown of miR-106a leaded to the attenuation of gastric cancer implantation capacity in vivo. Moreover, expression of TIMP2 was inversely associated with miR-106a in nodule tissues. Apoptotic body was also seen under electron microscope accompanied by silencing of miR-106a. Together, this data indicated that miR-106a may act as an oncogene and contribute to gastric cancer development.

Indexed as

AnimalsAntagomirsApoptosisCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceMicroRNAsNeoplasm MetastasisStomach NeoplasmsTissue Inhibitor of Metalloproteinase-2Xenograft Model Antitumor AssaysAntagomirsMicroRNAsMIRN106 microRNA, humanTIMP2 protein, humanTissue Inhibitor of Metalloproteinase-2FASGastric cancerMetastasisMicroRNA-106aTIMP2

Identifiers

PMID27142596
OpenAlexW2346635146

What OpenQuestion holds

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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.