Evidence map›Paper›PMID 25233933›Full record

ArticleMolecular cancer2014

OncomiR-196 promotes an invasive phenotype in oral cancer through the NME4-JNK-TIMP1-MMP signaling pathway.

Ya-Ching Lu, Joseph T Chang, Chun-Ta Liao, Chung-Jan Kang, Shiang-Fu Huang, I-How Chen, Chi-Che Huang, Yu-Chen Huang, Wen-Ho Chen, Chi-Ying Tsai and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

58 citing papers in PubMed, 142 citations in OpenAlex.

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  17. MicroRNA-31 Regulates Expression ofInternational journal of molecular sciences · 2020
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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

15 authors at 3 institutions in 2 countries.

Ya-Ching Lu
Joseph T Chang
Chun-Ta Liao
Chung-Jan Kang
Shiang-Fu Huang
I-How Chen
Chi-Che Huang
Yu-Chen Huang
Wen-Ho Chen
Chi-Ying Tsai
Hung-Ming Wang
Tzu-Chen Yen
Guo-Rung You
Chang-Hsu Chiang
Ann-Joy ChengDepartment of Medical Biotechnology, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Taoyuan, 333, Taiwan. annjoycheng@gap.cgu.edu.tw.
Chang Gung Memorial Hospital · TWChang Gung University · TWMemorial Hospital of South Bend · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNA-196 (miR-196), which is highly up-regulated in oral cancer cells, has been reported to be aberrantly expressed in several cancers; however, the significance of miR-196 in oral cancer has not yet been addressed.

methodsCellular functions in response to miR-196 modulation were examined, including cell growth, migration, invasion and radio/chemosensitivity. Algorithm-based studies were used to identify the regulatory target of miR-196. The miR-196 target gene and downstream molecular mechanisms were confirmed by RT-qPCR, western blot, luciferase reporter and confocal microscopy analyses. miR-196 expression was determined in paired cancer and adjacent normal tissues from oral cancer patients.

resultsBoth miR-196a and miR-196b were highly over-expressed in the cancer tissue and correlated with lymph node metastasis (P = 0.001 and P = 0.006, respectively). Functionally, miR-196 actively promoted cell migration and invasion without affecting cell growth. Mechanistically, miR-196 performed it's their function by inhibiting NME4 expression and further activating p-JNK, suppressing TIMP1, and augmenting MMP1/9.

conclusionmiR-196 contributes to oral cancer by promoting cell migration and invasion. Clinically, miR-196a/b was significantly over-expressed in the cancer tissues and correlated with lymph node metastasis. Thus, our findings provide new knowledge of the underlying mechanism of cancer metastasis. miR-196 may serve as a promising marker for better oral cancer management.

Indexed as

AdultAgedBase SequenceCell Line, TumorCell MovementCell ProliferationFemaleHumansJNK Mitogen-Activated Protein KinasesMaleMatrix MetalloproteinasesMicroRNAsMiddle AgedMolecular Sequence DataMouth NeoplasmsNeoplasm InvasivenessJNK Mitogen-Activated Protein KinasesMatrix MetalloproteinasesMicroRNAsMIRN196 microRNA, humanNME4 protein, humanNucleoside Diphosphate Kinase DTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID25233933
PMCPMC4176851
OpenAlexW2144893198

What OpenQuestion holds

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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.