Evidence map›Paper›PMID 29661252›Full record

ArticleCell communication and signaling : CCS2018

miR-148b-3p functions as a tumor suppressor in GISTs by directly targeting KIT.

Yu Wang, Jun Li, Dong Kuang, Xiaoyan Wang, Yuanli Zhu, Sanpeng Xu, Yaobing Chen, Henghui Cheng, Qiu Zhao, Yaqi Duan and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  10. Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022
    Review
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  13. Article
  14. Imatinib RegulatesInternational journal of molecular sciences · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Yu WangInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Jun LiInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Dong KuangInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Xiaoyan WangInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Yuanli ZhuInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Sanpeng XuInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Yaobing ChenInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Henghui ChengInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China.
Qiu ZhaoDepartment of Gastroenterology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, People's Republic of China.
Yaqi DuanInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China. yqduan@hust.edu.cn.ORCID 0000-0002-2392-5642
Guoping WangInstitute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Dadao, Wuhan, 430030, People's Republic of China. wanggp@hust.edu.cn.
Tongji Hospital · CNWuhan University · CN

Funding

National Natural Science Foundation of China 31271040National Natural Science Foundation of China 81000048National Natural Science Foundation of China 81270176National Natural Science Foundation of China 81300099National Natural Science Foundation of China 81302114National Natural Science Foundation of China 81600485
6 · The paper itself

Abstract

backgroundGain-of-function mutations and overexpression of KIT are characteristic features of gastrointestinal stromal tumor (GIST). Dysregulation in miRNA expression may lead to KIT overexpression and tumorigenesis.

methodsmiRNA microarray analysis and real-time PCR were used to determine the miRNA expression profiles in a cohort of 69 clinical samples including 50 CD117

resultsOf the six miRNAs whose expression was inversely correlated with that of KIT, we found that miR-148b-3p was significantly downregulated in the CD117

conclusionmiR-148b-3p functions as an important regulator of KIT expression and a potential prognostic biomarker for GISTs.

Indexed as

3' Untranslated RegionsAnimalsAntagomirsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationFemaleGastrointestinal NeoplasmsGastrointestinal Stromal TumorsHumansImatinib MesylateMaleMiceMice, Inbred BALB CMice, Nude3' Untranslated RegionsAntagomirsImatinib MesylateMicroRNAsMIRN148 microRNA, humanProto-Oncogene Proteins c-kitSTAT3 Transcription FactorGastrointestinal stromal tumor (GIST)KITmiR-148b-3pmiRNA

Identifiers

PMID29661252
PMCPMC5902930
OpenAlexW2800821587

What OpenQuestion holds

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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.