Evidence map›Paper›PMID 25961434›Full record

ArticleOncotarget2015

MiR-744 functions as a proto-oncogene in nasopharyngeal carcinoma progression and metastasis via transcriptional control of ARHGAP5.

Yuan Fang, Xiaoxia Zhu, Jian Wang, Na Li, Dianhe Li, Nazmus Sakib, Zhou Sha, Wen Song

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
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  15. p190RhoGAPs, theCells · 2019
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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 2 institutions in 1 country.

Yuan FangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaoxia ZhuDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jian WangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Na LiDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Dianhe LiDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nazmus SakibDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhou ShaDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wen SongDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a highly invasive and metastasis-prone epithelial cancer. The paucity of effective treatment strategies for recurrent and metastatic NPC is the major cause for stagnating survival rate of NPC. Therefore, it's urgent to understand the molecular mechanisms underlying NPC progression and identify novel avenues for targeted therapy. It has emerged recently that microRNAs are potential pro-tumorigenic or tumor-suppressive factors that participate in oncogenesis. In this study, we found that miR-744 expression was upregulated in NPC specimens compared to nasopharyngeal epithelium (NPE) tissue, and miR- 744 upregulation was significantly associated with TNM stage, tumorigenesis and metastasis. Functional studies revealed that miR-744 acts as a novel tumor promotor in NPC. Moreover, we determined that miR-744 targets ARHGAP5 (Rho GTPase activating protein 5), a protumorigenic gene, by directly interacting with its promoter and thereby regulating its expression at transcriptional level. Reintroduction of ARHGAP5 resembled the effects of miR-744 and silencing of ARHGAP5 clearly abrogated miR-744-induced enhancement of cell migration and invasion. High level of ARHGAP5 was positively correlated with that of miR-744 and with advanced stages of NPC, as well as with lymph node metastasis. Taken together, these data reveal for the first time that miR-744 exerts its proto-oncogenic function by directly targeting ARHGAP5 promoter. This newly identified miR-744/ARHGAP5 pathway provides further insight into the progression and metastasis of NPC and indicates potential novel therapeutic targets for NPC.

Indexed as

AnimalsCarcinomaCell Line, TumorDisease ProgressionGTPase-Activating ProteinsHumansMaleMiceMice, Inbred BALB CMicroRNAsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsProto-Oncogene MasProto-Oncogene ProteinsTranscription, GeneticARHGAP5 protein, humanGTPase-Activating ProteinsMAS1 protein, humanMicroRNAsMIRN744 microRNA, humanProto-Oncogene MasProto-Oncogene ProteinsARHGAP5metastasismiR-744nasopharyngeal carcinomatumorigenesis

Identifiers

PMID25961434
PMCPMC4537006
OpenAlexW1950856038

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.