Evidence map›Paper›PMID 30814512›Full record

ArticleCell death & disease2019

miR-215 suppresses papillary thyroid cancer proliferation, migration, and invasion through the AKT/GSK-3β/Snail signaling by targeting ARFGEF1.

Jihua Han, Meiyin Zhang, Chunlei Nie, Jinliang Jia, Fengyue Wang, Jiawei Yu, Wen Bi, Bo Liu, Ruinan Sheng, Guoqing He and 11 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. The Changing Face ofFrontiers in surgery · 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

21 authors at 3 institutions in 1 country.

Jihua HanDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Meiyin ZhangDepartment of Gynecology, Harbin Medical University Cancer Hospital, Harbin, China.
Chunlei NieDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Jinliang JiaDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Fengyue WangKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Jiawei YuDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Wen BiDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Bo LiuDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Ruinan ShengDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Guoqing HeDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Lingyu KongDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Lingling ZhengDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Rui PangDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Zhaoming DingDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Lili ChenDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Qiang GuanDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Shangha PanKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Xianzhi MengKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Jin XuDepartment of Cell Biology, Harbin Medical University, Harbin, China. xujinyd@aliyun.com.
Lianxin LiuKey Laboratory of Hepatosplenic Surgery, Ministry of Education, Department of General Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. liulx@ems.hrbmu.edu.cn.
Jiewu ZhangDepartment of Head and Neck Surgery, the Third Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. drzhangjiewu@sohu.com.
Third Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of papillary thyroid cancer (PTC) has been rapidly increasing in recent years. PTC is prone to lymph node metastasization, which further increases the recurrence rate and mortality of thyroid cancer. However, the underlying mechanisms of this process remain elusive. Several reports have shown that the microRNA miR-215 plays an important role in cancer metastasis. Here, we investigated, for the first time, the potential association between miR-215 and metastasis in PTC. The results of qPCR analysis demonstrated that miR-215 was downregulated in PTC cell lines and tissues, and lower levels of miR-215 correlated with lymph node metastasis of PTC. In vitro and in vivo assays revealed that restoration of miR-215 dramatically inhibited PTC cell proliferation and metastasis. We identified ADP ribosylation factor guanine nucleotide-exchange factor 1 (ARFGEF1) as the target, which mediated the function of miR-215. The expression of ARFGEF1 was inhibited by miR-215, and the effects of miR-215 were abrogated by re-expression of ARFGEF1. Moreover, we found that miR-215 suppressed PTC metastasis by modulating the epithelial-mesenchymal transition via the AKT/GSK-3β/Snail signaling. In summary, our study proves that miR-215 inhibits PTC proliferation and metastasis by targeting ARFGEF1 and indicates miR-215 as a biomarker for PTC prognosis.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDown-RegulationEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaGuanine Nucleotide Exchange FactorsHumansLymphatic MetastasisMaleMice, Inbred BALB CMice, NudeARFGEF1 protein, humanGlycogen Synthase Kinase 3 betaGuanine Nucleotide Exchange FactorsMicroRNAsMIRN215 microRNA, humanProto-Oncogene Proteins c-aktSNAI2 protein, humanSnail Family Transcription Factors

Identifiers

PMID30814512
PMCPMC6393497
OpenAlexW2915360666

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.