Evidence map›Paper›PMID 29023429›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

MiR-150 Inhibits Cell Growth In Vitro and In Vivo by Restraining the RAB11A/WNT/β-Catenin Pathway in Thyroid Cancer.

Dongfang Bai, Haipeng Sun, Xiaodong Wang, Hongliang Lou, Jian Zhang, Xiaohong Wang, Ling Jiang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 34 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

7 authors at 2 institutions in 1 country.

Dongfang BaiDepartment of Endocrinology, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Haipeng SunDepartment of Emergency, Tai'an Central Hospital, Tai'an, Shandong, China (mainland).
Xiaodong WangDepartment of Nephrology, Tai'an Central Hospital, Tai'an, Shandong, China (mainland).
Hongliang LouDepartment of Ultrasound, People's Hospital of Dongping, Tai'an, Shandong, China (mainland).
Jian ZhangDepartment of Endocrinology, Tai'an Central Hospital, Tai'an, Shandong, China (mainland).
Xiaohong WangDepartment of Gastroenterology, Tai'an Central Hospital, Tai'an, Shandong, China (mainland).
Ling JiangDepartment of Endocrinology, Qilu Hospital, Shandong University, Jinan, Shandong, China (mainland).
Taian City Central Hospital · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Emerging evidence has shown that downregulation or upregulation of microRNAs (miRNAs) plays an important role in the development and progression of thyroid cancer (TC). However, the potential role of miR-150 and its biological function in TC remains largely unclear. MATERIAL AND METHODS Real-time polymerase chain reaction (RT-qPCR) was employed to detect the expression level of miR-150 and RAB11A in human TC tissue and human normal thyroid tissue. MTT assay, colony formation assay, flow cytometry cell cycle, and apoptosis assay were used to investigate the role of miR-150 and RAB11A on the malignant phenotypes in vitro. Nude mouse xenograft assay and western blot assay was used to verify the function of miR-150 in vivo. Western blot assay and immunofluorescence assay were used to detect the activation of WNT/β-catenin pathway mediated by miR-150 and RAB11A. EGFP reporter assay, RT-qPCR assay, and western blot assay were used to validate the regulation relationship. RESULTS This study demonstrated that miR-150 expression in human TC tissues was markedly downregulated. Moreover, overexpression of miR-150 markedly inhibited cell proliferation via inducing the cell cycle arrest and promoting cell apoptosis by directly targeting RAB11A in vitro and suppressing tumor growth in vivo. However, overexpression of RAB11A promoted cell malignant phenotypes. In addition, miR-150 restrained the RAB11A mediated WNT/β-catenin activation in TC cells. CONCLUSIONS miR-150 may function as a suppressor gene in TC cells by inhibiting the RAB11A/WNT/β-catenin pathway.

Indexed as

AnimalsApoptosisbeta CateninCell CycleCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticHumansMiceMice, NudeMicroRNAsrab11 GTP-Binding Proteinsrab GTP-Binding Proteinsbeta CateninMicroRNAsMIR150, humanrab11 GTP-Binding Proteinsrab GTP-Binding Proteins

Identifiers

PMID29023429
PMCPMC5649516
OpenAlexW2763026025

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.