Evidence map›Paper›PMID 24816813›Full record

ArticlePloS one2014

MicroRNA-133a suppresses multiple oncogenic membrane receptors and cell invasion in non-small cell lung carcinoma.

Lu-Kai Wang, Tzu-Hung Hsiao, Tse-Ming Hong, Hsuan-Yu Chen, Shih-Han Kao, Wen-Lung Wang, Sung-Liang Yu, Ching-Wen Lin, Pan-Chyr Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 3 pooled it
4.8field-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

40 citing papers in PubMed, 3 syntheses or guidelines pooled it, 82 citations in OpenAlex.

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  18. Gut and liver · 2018
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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

9 authors at 5 institutions in 1 country.

Lu-Kai WangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
Tzu-Hung HsiaoDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Tse-Ming HongInstitute of Clinical Medicine, National Cheng Kung University, Tainan, Taiwan.
Hsuan-Yu ChenInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
Shih-Han KaoDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wen-Lung WangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Sung-Liang YuDepartment of Clinical Laboratory Sciences and Medical Biotechnology College of Medicine, National Taiwan University, Taipei, Taiwan; NTU Center of Genomic Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ching-Wen LinInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Pan-Chyr YangGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan; Department of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; NTU Center of Genomic Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
National Taiwan University · TWInstitute of Biomedical Sciences, Academia Sinica · TWNational Defense Medical Center · TWInstitute of Statistical Science, Academia Sinica · TWNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancers (NSCLCs) cause high mortality worldwide, and the cancer progression can be activated by several genetic events causing receptor dysregulation, including mutation or amplification. MicroRNAs are a group of small non-coding RNA molecules that function in gene silencing and have emerged as the fine-tuning regulators during cancer progression. MiR-133a is known as a key regulator in skeletal and cardiac myogenesis, and it acts as a tumor suppressor in various cancers. This study demonstrates that miR-133a expression negatively correlates with cell invasiveness in both transformed normal bronchial epithelial cells and lung cancer cell lines. The oncogenic receptors in lung cancer cells, including insulin-like growth factor 1 receptor (IGF-1R), TGF-beta receptor type-1 (TGFBR1), and epidermal growth factor receptor (EGFR), are direct targets of miR-133a. MiR-133a can inhibit cell invasiveness and cell growth through suppressing the expressions of IGF-1R, TGFBR1 and EGFR, which then influences the downstream signaling in lung cancer cell lines. The cell invasive ability is suppressed in IGF-1R- and TGFBR1-repressed cells and this phenomenon is mediated through AKT signaling in highly invasive cell lines. In addition, by using the in vivo animal model, we find that ectopically-expressing miR-133a dramatically suppresses the metastatic ability of lung cancer cells. Accordingly, patients with NSCLCs who have higher expression levels of miR-133a have longer survival rates compared with those who have lower miR-133a expression levels. In summary, we identified the tumor suppressor role of miR-133a in lung cancer outcome prognosis, and we demonstrated that it targets several membrane receptors, which generally produce an activating signaling network during the progression of lung cancer.

Indexed as

Carcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDown-RegulationGene Knockdown TechniquesHumansLung NeoplasmsMicroRNAsNeoplasm InvasivenessNeoplasm MetastasisOncogene ProteinsPrognosisProto-Oncogene Proteins c-aktReceptors, Cell SurfaceSignal TransductionMicroRNAsMIRN133 microRNA, humanOncogene ProteinsProto-Oncogene Proteins c-aktReceptors, Cell Surface

Identifiers

PMID24816813
PMCPMC4016005
OpenAlexW1984235695

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.