Evidence map›Paper›PMID 31557058›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Long noncoding RNA SMAD5-AS1 acts as a microRNA-106a-5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma.

Ying-Juan Zheng, Jing-Yi Zhao, Tian-Song Liang, Ping Wang, Juan Wang, Dao-Ke Yang, Zhang-Suo Liu

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Increased expression of SMAD5-AS1 in glioma is associated with patient prognosis and immunity.International journal of clinical and experimental pathology · 2026
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  18. Long non-coding RNABioengineered · 2021
    Article
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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 1 institution in 1 country.

Ying-Juan ZhengDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jing-Yi ZhaoDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Tian-Song LiangDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Ping WangDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Juan WangDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Dao-Ke YangDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhang-Suo LiuDepartment of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a malignant epithelial cancer of the head and neck with high prevalence in southern China, which is accompanied by notable invasiveness and metastasis. Long noncoding RNAs (lncRNAs) participate in the progression of various cancers including NPC. Microarray-based analysis identified highly expressed lncRNA mothers against decapentaplegic homolog 5 (SMAD5)-antisense RNA 1 (AS1) related to NPC. Interestingly, it is found that SMAD5-AS1 competitively bound to microRNA (miR)-106a-5p to regulate SMAD5. Herein, the study aimed to clarify the role of SMAD5-AS1/miR-106a-5p/SMAD5 axis in the process of epithelial mesenchymal transition (EMT) in NPC. SMAD5-AS1 was highly expressed and miR-106a-5p was poorly expressed in NPC tissues and cell lines. The NPC cells were treated with a series of small interfering RNAs, mimics, or inhibitors to explore the effects of SMAD5-AS1, SMAD5, and miR-106a-5p on EMT, cell proliferation, migration, and invasion in NPC. Of note, SMAD5-AS1 silencing or miR-106a-5p overexpression reduced expression of N-cadherin, matrix metallopeptidase 9, Snail, and Vimentin while elevating E-cadherin expression, thus inhibiting EMT, cell proliferation, migration, and invasion in NPC by down-regulation of SMAD5. Moreover, SMAD5 silencing could reduce the ability of EMT induced by SMAD5-AS1 up-regulation. SMAD5-AS1 silencing or miR-106a-5p elevation inhibited tumorigenesis in nude mice. Taken together, SMAD5-AS1 silencing suppressed EMT, cell proliferation, migration, and invasion in NPC by elevating miR-106a-5p to down-regulate SMAD5, which provided a novel therapeutic target for NPC treatment.-Zheng, Y.-J., Zhao, J.-Y., Liang, T.-S., Wang, P., Wang, J., Yang, D.-K., Liu, Z.-S. Long noncoding RNA SMAD5-AS1 acts as a microRNA-106a-5p sponge to promote epithelial mesenchymal transition in nasopharyngeal carcinoma.

Indexed as

CarcinogenesisCell Line, TumorEpithelial-Mesenchymal TransitionGene SilencingHumansMicroRNAsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsRNA, Long NoncodingTranscription FactorsMicroRNAsMIRN106 microRNA, humanRNA, Long NoncodingSMAD5-AS1 lncRNA, humanTranscription FactorsceRNAinvasionmigrationproliferationSMAD5

Identifiers

PMID31557058
PMCPMC6902713
OpenAlexW2976586930

What OpenQuestion holds

Textmetadata
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.