Evidence map›Paper›PMID 29540201›Full record

ArticleJournal of experimental & clinical cancer research : CR2018

Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway.

Min Sha, Mei Lin, Jia Wang, Jun Ye, Jie Xu, Ning Xu, Junxing Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.3field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

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  6. Role of Extracellular Vesicles in TSC Renal Cystogenesis.International journal of molecular sciences · 2025
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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

7 authors at 2 institutions in 1 country.

Min ShaInstitute of Clinical medicine, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Mei LinInstitute of Clinical medicine, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Jia WangDepartment of Reproductive Medicine, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Jun YeInstitute of Clinical medicine, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Jie XuInstitute of Clinical medicine, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Ning XuDepartment of Gastroenterology, Taizhou people's Hospital affiliated of Nantong University of medicine, Taizhou, China.
Junxing HuangInstitute of Oncology, Taizhou people's Hospital affiliated of Nantong University of medicine, 210 Yingchun, Taizhou, Jiangsu Province, 225300, China. tzrmyy5211@163.com.
Nantong University · CNTaizhou People's Hospital · CN

Funding

333 Plan Foundation of Jiangsu BRA2017173Jiangsu Provincial Medical Innovation Team CXTDA2017042National Natural Science Foundation of China 81571797Taizhou people's Hospital ZL201617
6 · The paper itself

Abstract

backgroundThe objective of this study was to investigate the role and mechanism of long non-coding RNA MIAT in gastric cancer (GC).

methodsReal-time PCR was used to determine MIAT level in 120 GC tissues, and in two gastric cancer cell lines. The clinicopathological characteristics of MIAT in GC patients were analyzed. Small interfering RNA specific for MIAT (si-MIAT) and lentivector for si-MIAT was performed to down-regulate MIAT expression in GC cells and in animal tumor model, respectively. The interaction of MIAT and miR-141 was measured by RNA pull-down assay and RNA immunoprecipitation. The biological function of si-MIAT on GC cell growth and metastasis were explored through flow cytometry assay, invasion and migration assay in vitro.

resultsMIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis. MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo. Furthermore, MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression. In BGC-823 and MGC-803 cells with si-MIAT, DDX5 overexpression resulted in an increase of cell proliferation, migration and invasion.

conclusionsOur data indicated that MIAT played an oncogenic role in GC growth and metastasis, and could serve as a novel molecular target for treating GC.

Indexed as

Gene Expression Regulation, NeoplasticRNA Interference3' Untranslated RegionsAdultAgedAged, 80 and overAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationDEAD-box RNA HelicasesDisease Models, AnimalFemaleGene Knockdown TechniquesGenes, Reporter3' Untranslated RegionsDdx5 protein, humanDEAD-box RNA HelicasesMiat long non-coding RNAMicroRNAsMIRN141 microRNA, humanRNA, Long NoncodingDDX5Gastric cancerMIATmiR-141

Identifiers

PMID29540201
PMCPMC5852965
OpenAlexW2801911148

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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.