Evidence map›Paper›PMID 26364844›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

miR-221 and miR-222 Simultaneously Target RECK and Regulate Growth and Invasion of Gastric Cancer Cells.

Wenneng Liu, Nian Song, Huihua Yao, Liying Zhao, Hao Liu, Guoxin Li

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  6. Function of Non-coding RNA inFrontiers in molecular biosciences · 2021
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  16. miR-222 induces Adriamycin resistance in breast cancer through PTEN/Akt/p27Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

6 authors at 2 institutions in 1 country.

Wenneng LiuDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Nian SongDepartment of General Surgery, The First People's Hospital of Chengdu, Chengdu, Sichuan, China (mainland).
Huihua YaoDepartment of General Surgery, The First People's Hospital of Chengdu, Chengdu, Sichuan, China (mainland).
Liying ZhaoDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Hao LiuDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Guoxin LiDepartment of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China (mainland).
Southern Medical University · CNChengdu Women's and Children's Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough Helicobacter pylori infection is necessary for development of gastric adenocarcinoma (GAC), the underlying mechanism remains poorly defined. This study aimed to explore how miR-221 and miR-222 are dysregulated after H. pylori infection and how these 2 miRNAs are involved in pathological development of gastric cancer. MATERIAL AND

methodsqRT-PCR analysis was performed to quantify miR-221 and miR-222 expression in patients with H. pylori - induced chronic gastritis, H. pylori-negative healthy controls, and in gastric cancer tissues and the corresponding adjacent normal tissues. Cell models were used to verify the expression profile. Dual luciferase assay was performed to verify putative binding between miR-221 or miR-222 and RECK. A loss-and-gain function study was performed to assess the miR-221/miR-222-RECK axis in gastric cancer cells.

resultsH. pylori infection leads to significantly higher miR-221 and miR-222 expression. MiR-221 and miR-222 can bind the same sequence of RECK 3'UTR, thereby modulating its expression. Through simultaneous regulation over RECK, miR-221 and miR-222 can promote gastric cancer cell growth and invasion.

conclusionsThe miR-221/miR-222-RECK axis might be an important path modulating H. pylori infection-related gastric cancer development.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdenocarcinomaAdultCell SurvivalCell Transformation, NeoplasticFemaleFlow CytometryGPI-Linked ProteinsHEK293 CellsHelicobacter InfectionsHelicobacter pyloriHumansMaleMicroRNAsMiddle Aged3' Untranslated RegionsGPI-Linked ProteinsMicroRNAsMIR221, humanMIR222, humanRECK protein, human

Identifiers

PMID26364844
PMCPMC4576921
OpenAlexW2222651771

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.