Evidence map›Paper›PMID 29416000›Full record

ArticleCell death & disease2018

miR-195 targets cyclin D3 and survivin to modulate the tumorigenesis of non-small cell lung cancer.

Xiaojie Yu, Yiqiang Zhang, David Cavazos, Xiuye Ma, Zhenze Zhao, Liqin Du, Alexander Pertsemlidis

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.6field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  16. Bioinformatics analysis of BIRC5 in human cancers.Annals of translational medicine · 2022
    Article
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  19. LncRNATranslational cancer research · 2022
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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.

Xiaojie YuGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Yiqiang ZhangGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
David CavazosGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Xiuye MaGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Zhenze ZhaoDepartment of Chemistry and Biochemistry, Texas State University at San Marcos, San Marcos, TX, USA.
Liqin DuDepartment of Chemistry and Biochemistry, Texas State University at San Marcos, San Marcos, TX, USA.
Alexander PertsemlidisGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. pertsemlidis@uthscsa.edu.ORCID 0000-0003-1624-9372
The University of Texas Health Science Center at San Antonio · USTexas State University · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Robin Jean Leach · 1991 to 2026
$59.1M
microRNA regulation of drug sensitivity in non-small cell lung cancerR01CA129632 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI PERTSEMLIDIS, ALEXANDER · 2007 to 2011
$1.6M
NCI NIH HHS P30 CA054174NCI NIH HHS R01 CA129632
6 · The paper itself

Abstract

miR-195 has recently been reported to function as a tumor suppressor in various cancers, including non-small cell lung cancer (NSCLC). However, the mechanisms by which miR-195 represses the tumorigenesis of NSCLC cells are not fully understood. We performed a high-throughput screen using an miRNA mimic library and confirmed the identification of miR-195 as a tumor suppressor in NSCLC. We demonstrated that overexpression or induced expression of miR-195 in lung tumors slows tumor growth and that repression of miR-195 accelerates tumor growth. In addition, we found that knockout of miR-195 promotes cancer cell growth. We demonstrated that miR-195 targets cyclin D3 to cause cell cycle arrest at the G1 phase and that miR-195 targets survivin to induce apoptosis and senescence in NSCLC cells. Overexpression of cyclin D3 or survivin reverses the effects of miR-195 in NSCLC cells. Through the analysis of data from The Cancer Genome Atlas, we confirmed that the expression of miR-195 is lower in tumors than in adjacent normal tissues and that low expression of miR-195 is associated with poor survival in both lung adenocarcinoma and squamous cell carcinoma patients. Specifically, we found that BIRC5, which codes for survivin, is upregulated in both adenocarcinoma and squamous cell carcinoma tissues and that high expression of BIRC5 is associated with poor survival in adenocarcinoma, but not squamous cell carcinoma. In addition, the ratio of miR-195 level to BIRC5 level is associated with both recurrence-free and overall survival in lung adenocarcinoma. Our results suggest that the miR-195/BIRC5 axis is a potential target for treatment of lung adenocarcinoma specifically, and NSCLC in general.

Indexed as

AnimalsCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCyclin D3FemaleHeterograftsHumansLung NeoplasmsMiceMice, NudeMicroRNAsSurvival AnalysisSurvivinTransfectionBIRC5 protein, humanCCND3 protein, humanCyclin D3MicroRNAsMIRN195 microRNA, humanSurvivin

Identifiers

PMID29416000
PMCPMC5833354
OpenAlexW2793353518

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.