Evidence map›Paper›PMID 26451614›Full record

ArticleOncotarget2015

MiR-573 inhibits prostate cancer metastasis by regulating epithelial-mesenchymal transition.

Lin Wang, Guanhua Song, Weiwei Tan, Mei Qi, Lili Zhang, Jonathan Chan, Jindan Yu, Jinxiang Han, Bo Han

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 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.9field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

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  13. miR-573 suppresses pancreatic cancer cell proliferation, migration, and invasion through targeting TSPAN1.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 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

9 authors at 6 institutions in 3 countries.

Lin WangResearch Center for Medicinal Biotechnology, Key Laboratory for Rare & Uncommon Diseases of Shandong Province, Shandong Academy of Medicinal Sciences, Jinan, China.
Guanhua SongInstitute of Basic Medicine, Shandong Academy of Medical Sciences, Jinan, China.
Weiwei TanDepartment of Pathology, Shandong University Medical School, Jinan, China.
Mei QiDepartment of Pathology, Shandong University Medical School, Jinan, China.
Lili ZhangDepartment of Pathology, Shandong University Medical School, Jinan, China.
Jonathan ChanDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada.
Jindan YuDivision of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Jinxiang HanResearch Center for Medicinal Biotechnology, Key Laboratory for Rare & Uncommon Diseases of Shandong Province, Shandong Academy of Medicinal Sciences, Jinan, China.
Bo HanDepartment of Pathology, Shandong University Medical School, Jinan, China.
Shandong University · CNShandong Academy of Pharmaceutical Sciences · CNNorthwestern University · USQilu Hospital of Shandong University · CNShandong First Medical University · CNUniversity of Toronto · CA

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
NCI NIH HHS P30 CA060553
6 · The paper itself

Abstract

The metastastic cascade is a complex process that is regulated at multiple levels in prostate cancer (PCa). Recent evidence suggests that microRNAs (miRNAs) are involved in PCa metastasis and hold great promise as therapeutic targets. In this study, we found that miR-573 expression is significantly lower in metastatic tissues than matched primary PCa. Its downregulation is correlated with high Gleason score and cancer-related mortality of PCa patients (P = 0.041, Kaplan-Meier analysis). Through gain- and loss-of function experiments, we demonstrated that miR-573 inhibits PCa cell migration, invasion and TGF-β1-induced epithelial-mesenchymal transition (EMT) in vitro and lung metastasis in vivo. Mechanistically, miR573 directly targets the fibroblast growth factor receptor 1 (FGFR1) gene. Knockdown of FGFR1 phenocopies the effects of miR-573 expression on PCa cell invasion, whereas overexpression of FGFR1 partially attenuates the functions of miR-573. Consequently, miR-573 modulates the activation of FGFR1-downstream signaling in response to fibroblast growth factor 2 (FGF2). Importantly, we showed that GATA3 directly increases miR-573 expression, and thus down-regulates FGFR1 expression, EMT and invasion of PCa cells in a miR-573-dependent manner, supporting the involvement of GATA3, miR-573 and FGFR1 in controlling the EMT process during PCa metastasis. Altogether, our findings demonstrate a novel mechanism by which miR-573 modulates EMT and metastasis of PCa cells, and suggest miR-573 as a potential biomarker and/or therapeutic target for PCa management.

Indexed as

AnimalsCell Line, TumorEpithelial-Mesenchymal TransitionHEK293 CellsHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsMiddle AgedNeoplasm MetastasisProstatic NeoplasmsTransfectionMicroRNAsMIRN573 microRNA, humanFGFR1GATA3metastasismiR-573prostate cancer

Identifiers

PMID26451614
PMCPMC4742155
OpenAlexW2120346211

What OpenQuestion holds

Textmetadata
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.