Evidence map›Paper›PMID 25873390›Full record

ArticleThe Journal of biological chemistry2015

Autocrine/Paracrine Human Growth Hormone-stimulated MicroRNA 96-182-183 Cluster Promotes Epithelial-Mesenchymal Transition and Invasion in Breast Cancer.

Weijie Zhang, Pengxu Qian, Xiao Zhang, Min Zhang, Hong Wang, Mingming Wu, Xiangjun Kong, Sheng Tan, Keshuo Ding, Jo K Perry and 4 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025
    Review
  4. miR-96-5p expression is sufficient to induce and maintain the senescent cell fate in the absence of stress.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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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

14 authors at 4 institutions in 3 countries.

Weijie ZhangFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China, the Hefei National Laboratory for Physical Sciences at Microscale, Hefei, Anhui 230027, China.
Pengxu QianFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiao ZhangFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Min ZhangFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China, the Hefei National Laboratory for Physical Sciences at Microscale, Hefei, Anhui 230027, China.
Hong WangFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Mingming WuFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Xiangjun KongFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Sheng TanFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Keshuo DingFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China.
Jo K Perrythe Liggins Institute and Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland 1023, New Zealand.
Zhengsheng WuFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China, the Department of Pathology, Anhui Medical University, Hefei, Anhui 230027, China, and.
Yuan Caothe Department of Pathology, Anhui Medical University, Hefei, Anhui 230027, China, and.
Peter E Lobiethe Cancer Science Institute of Singapore and Department of Pharmacology, National University of Singapore, Singapore 117599, Singapore csipel@nus.edu.sg.
Tao ZhuFrom the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China, the Hefei National Laboratory for Physical Sciences at Microscale, Hefei, Anhui 230027, China, zhut@ustc.edu.cn.
University of Science and Technology of China · CNAnhui Medical University · CNMaurice Wilkins Centre · NZNational University Cancer Institute, Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human growth hormone (hGH) plays critical roles in pubertal mammary gland growth, development, and sexual maturation. Accumulated studies have reported that autocrine/paracrine hGH is an orthotopically expressed oncoprotein that promotes normal mammary epithelial cell oncogenic transformation. Autocrine/paracrine hGH has also been reported to promote mammary epithelial cell epithelial-mesenchymal transition (EMT) and invasion. However, the underlying mechanism remains largely obscure. MicroRNAs (miRNAs) are reported to be involved in regulation of multiple cellular functions of cancer. To determine whether autocrine/paracrine hGH promotes EMT and invasion through modulation of miRNA expression, we performed microarray profiling using MCF-7 cells stably expressing wild type or a translation-deficient hGH gene and identified miR-96-182-183 as an autocrine/paracrine hGH-regulated miRNA cluster. Forced expression of miR-96-182-183 conferred on epithelioid MCF-7 cells a mesenchymal phenotype and promoted invasive behavior in vitro and dissemination in vivo. Moreover, we observed that miR-96-182-183 promoted EMT and invasion by directly and simultaneously suppressing BRMS1L (breast cancer metastasis suppressor 1-like) gene expression. miR-96 and miR-182 also targeted GHR, providing a potential negative feedback loop in the hGH-GHR signaling pathway. We further demonstrated that autocrine/paracrine hGH stimulated miR-96-182-183 expression and facilitated EMT and invasion via STAT3 and STAT5 signaling. Consistent with elevated expression of autocrine/paracrine hGH in metastatic breast cancer tissue, miR-96-182-183 expression was also remarkably enhanced. Hence, we delineate the roles of the miRNA-96-182-183 cluster and elucidate a novel hGH-GHR-STAT3/STAT5-miR-96-182-183-BRMS1L-ZEB1/E47-EMT/invasion axis, which provides further understanding of the mechanism of autocrine/paracrine hGH-stimulated EMT and invasion in breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHuman Growth HormoneHumansIn Situ HybridizationMiceMice, Inbred BALB CMice, NudeMicroRNAsMicroscopy, ConfocalMicroscopy, FluorescenceBRMS1 protein, humanHuman Growth HormoneMicroRNAsMirn182 microRNA, humanMIRN183 microRNA, humanMIRN96 microRNA, humanRepressor ProteinsRNA, Small Interferingbreast cancerBRMS1Lepithelial-mesenchymal transition (EMT)growth hormoneinvasionmicroRNA (miRNA)miR-96-182-183 cluster

Identifiers

PMID25873390
PMCPMC4447958
OpenAlexW1970094205

What OpenQuestion holds

Textmetadata
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.