Evidence map›Paper›PMID 25663460›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015

miR-342-3p targets RAP2B to suppress proliferation and invasion of non-small cell lung cancer cells.

Xiao Xie, Hongtao Liu, Mingsong Wang, Fangbao Ding, Haibo Xiao, Fengqing Hu, Rui Hu, Ju Mei

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  4. DF-MDA: An effective diffusion-based computational model for predicting miRNA-disease association.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
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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

8 authors at 3 institutions in 1 country.

Xiao XieDepartment of Cardio-thoracic Surgery, Xinhua Hospital, School of Medicine, Shanghai JiaoTong University, Shanghai, 200092, China.
Hongtao Liu
Mingsong Wang
Fangbao Ding
Haibo Xiao
Fengqing Hu
Rui Hu
Ju Mei
Shanghai Jiao Tong University · CNXinHua Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) play critical roles in cancer development and progression. In this study, we examined the roles and molecular mechanisms of miR-342-3p in human non-small cell lung cancer (NSCLC). The results showed that miR-342-3p is downregulated in NSCLC cell lines and tissues, and its overexpression induces significant inhibition of NSCLC cell proliferation, invasion, and tumor growth in nude mice. In addition, miR-342-3p repressed RAP2B expression through interactions with its 3'-UTR region. Restoration of RAP2B expression reversed miR-342-3p-mediated inhibitory activity in NSCLC cells. Finally, analyses of miR-342-3p and RAP2B levels in NSCLCs revealed that miR-342-3p inversely correlated with RAP2B mRNA expression. Our collective findings provide preliminary evidence that miR-342-3p acts as a tumor suppressor in NSCLC through repression of RAP2B.

Indexed as

3' Untranslated RegionsAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceMicroRNAsNeoplasm Invasivenessrap GTP-Binding ProteinsXenograft Model Antitumor Assays3' Untranslated RegionsMicroRNAsMIRN342 microRNA, humanRAP2B protein, humanrap GTP-Binding Proteins

Identifiers

PMID25663460
OpenAlexW2041817403

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.