Evidence map›Paper›PMID 28650464›Full record

ArticleOncogene2017

β-catenin downregulates Dicer to promote ovarian cancer metastasis.

S K Y To, A S C Mak, Y M Eva Fung, C-M Che, S-S Li, W Deng, B Ru, J Zhang, A S T Wong

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

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  19. MicroRNA-892a regulates laryngocarcinoma cell proliferation via Dicer.Experimental biology and medicine (Maywood, N.J.) · 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

9 authors at 2 institutions in 2 countries.

S K Y ToSchool of Biological Sciences, University of Hong Kong, Hong Kong.
A S C MakSchool of Biological Sciences, University of Hong Kong, Hong Kong.
Y M Eva FungDepartment of Chemistry, Chemical Biology Centre, State Key Laboratory of Synthetic Chemistry, University of Hong Kong, Hong Kong.
C-M CheDepartment of Chemistry, Chemical Biology Centre, State Key Laboratory of Synthetic Chemistry, University of Hong Kong, Hong Kong.
S-S LiSchool of Biological Sciences, University of Hong Kong, Hong Kong.
W DengSchool of Nursing, University of Hong Kong, Hong Kong.
B RuSchool of Biological Sciences, University of Hong Kong, Hong Kong.
J ZhangSchool of Biological Sciences, University of Hong Kong, Hong Kong.
A S T WongSchool of Biological Sciences, University of Hong Kong, Hong Kong.
University of Hong Kong · HKState Key Laboratory of Synthetic Chemistry · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is a nearly uniform lethal disease and its highly aggressive metastatic phenotype portends a poor prognosis. Lack of a well-controlled, relevant experimental model has been a major obstacle to identifying key molecules causing metastasis. Here we describe the creation of a new isogenic model of spontaneous human ovarian cancer metastasis exhibiting opposite phenotypes-highly metastatic (HM) and non-metastatic (NM)-both in vitro and in vivo. HM was unique in its ability to metastasize consistently to the peritoneum, mimicking the major dissemination route of human ovarian cancer. In contrast, NM failed to form detectable metastases, although it was equally tumorigenic. Using comparative label-free quantitative liquid chromatography tandem mass spectrometry (LC-MS/MS), we identified β-catenin, which we demonstrated for the first time as having a direct role in the pathogenesis of ovarian cancer metastasis. Our studies also revealed a previously unrecognized role of β-catenin in the downregulation of multiple microRNAs (miRNAs) through attenuating miRNA biogenesis by targeting Dicer, a key component of the miRNA-processing machinery. One such downregulated miRNAs was miR-29s involved in epithelial-to-mesenchymal transition and subsequent stem cell traits. Silencing β-catenin or overexpressing Dicer or miR-29 mimics in HM significantly reduced the ability of these cells to migrate. β-catenin-knockdown cells also failed to metastasize in an orthotopic model of ovarian cancer. Meta-analysis revealed an increase in CTNNB1 and a decrease in DICER1 expression levels in the high-risk group. These results uncover β-catenin as a critical factor in promoting ovarian cancer aggressiveness and a new mechanism linking between β-catenin and miRNA downregulation underlying this process.

Indexed as

Animalsbeta CateninCarcinogenesisCell Line, TumorCell ProliferationChromatography, LiquidDEAD-box RNA HelicasesEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMiceMicroRNAsNeoplasm MetastasisOvarian NeoplasmsRibonuclease IIIbeta CateninCTNNB1 protein, humanDEAD-box RNA HelicasesDICER1 protein, humanMicroRNAsMIRN29a microRNA, humanRibonuclease III

Identifiers

PMID28650464
OpenAlexW2635073344

What OpenQuestion holds

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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.