Evidence map›Paper›PMID 32336285›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

miR-615-3p promotes the epithelial-mesenchymal transition and metastasis of breast cancer by targeting PICK1/TGFBRI axis.

Bo Lei, Dandan Wang, Ming Zhang, Yuwei Deng, Huijie Jiang, Yiwen Li

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 89 citations in OpenAlex.

  1. Research progress on the regulation of miRNAs in diabetic kidney disease and osteoporosis.International journal of clinical and experimental pathology · 2026
    Review
  2. Noncoding RNAs, Vital Players in Breast Cancer Metastasis.Breast cancer (Dove Medical Press) · 2025
    Review
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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

6 authors at 3 institutions in 1 country.

Bo LeiDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150086, China.
Dandan WangDepartment of Radiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150086, China.
Ming ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150086, China.
Yuwei DengDepartment of Oncology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150086, China.
Huijie JiangDepartment of Radiology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150086, China. jianghuijie@hrbmu.edu.cn.
Yiwen LiDepartment of Oncology, The Second Affiliated Hospital of Harbin Medical University, 246 Xuefu Road, Harbin, 150086, China. zlylyw@126.com.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence indicates that epithelial-mesenchymal transition (EMT) can be regulated by microRNAs (miRNAs). miR-615-3p was shown to be involved in tumor development. However, the role of miR-615-3p in the metastasis of breast cancer remains largely unknown.

methodsThe expression of miR-615-3p in breast cancer cells and tissues was assessed by qRT-PCR and situ hybridization assays. Effects of miR-615-3p on tumor metastasis were evaluated with experiments in vitro and mouse model. EMT markers were detected by western blot and immunofluorescence assays. Molecular mechanism of miR-615-3p in the regulation of breast cancer cell metastasis was analyzed by Western Blot, Co-immunoprecipitation, and Luciferase assay.

resultsIn the present study, we found that miR-615-3p was significantly elevated in breast cancer cells and tissues, especially in those with metastasis. In breast cancer cell lines, stable overexpression of miR-615-3p was sufficient to promote cell motility in vitro, and pulmonary metastasis in vivo, accompanied by the reduced expression of epithelial markers and the increased levels of mesenchymal markers. Further studies revealed that the reintroduction of miR-615-3p increased the downstream signaling of TGF-β, the type I receptor (TGFBRI) by targeting the 3'-untranslated regions (3'-UTR) of PICK1. PICK1 inhibits the binding of DICER1 to Smad2/3 and the processing of pre-miR-615-3p to mature miR-615-3p in breast cancer cells, thus exerting a negative feedback loop.

conclusionsOur data highlight an important role of miR-615-3p in the molecular etiology of breast cancer, and implicate the potential application of miR-615-3p in cancer therapy.

Indexed as

AnimalsBreast NeoplasmsCarrier ProteinsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHEK293 CellsHeterograftsHumansMCF-7 CellsMiceMice, NudeMicroRNAsNeoplasm MetastasisNuclear ProteinsReceptor, Transforming Growth Factor-beta Type ICarrier ProteinsMicroRNAsMIRN615 microRNA, humanNuclear ProteinsPICk1 protein, humanReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanBreast cancerEMTmiR-615-3pPICK1TGF-β

Identifiers

PMID32336285
PMCPMC7183699
OpenAlexW3019972887

What OpenQuestion holds

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LicenceCC BY
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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.