Evidence map›Paper›PMID 28628113›Full record

ArticleOncogene2017

MicroRNA-20a-mediated loss of autophagy contributes to breast tumorigenesis by promoting genomic damage and instability.

L Liu, J He, X Wei, G Wan, Y Lao, W Xu, Z Li, H Hu, Z Hu, X Luo and 4 more

Open access · hybridAbstract read
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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 88 citations in OpenAlex.

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  17. Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022
    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 3 institutions in 1 country.

L LiuSchool of Life Sciences, Tsinghua University, Beijing, China.
J HeKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.ORCID 0000-0002-5880-8112
X WeiKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
G WanSchool of Life Sciences, Tsinghua University, Beijing, China.
Y LaoSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.ORCID 0000-0002-7803-4484
W XuSchool of Life Sciences, Tsinghua University, Beijing, China.
Z LiSchool of Chemical Biology and Biotechnology, Graduate School at Shenzhen, Peking University, Shenzhen, China.
H HuDepartment of Breast Surgery, Peking University Shenzhen Hospital, Shenzhen, China.
Z HuDepartment of Clinical Oncology, Wuhan No. 1 Hospital, Wuhan, China.
X LuoKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
J WuSchool of Life Sciences, Tsinghua University, Beijing, China.
W XieKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
Y ZhangKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
N XuKey Lab in Healthy Science and Technology, Division of Life Science, Graduate School at Shenzhen, Tsinghua University, Shenzhen, China.
University Town of Shenzhen · CNShanghai University of Traditional Chinese Medicine · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene expression analysis of The Cancer Genome Atlas (TCGA) breast cancer data set show that miR-20a is upregulated in human breast cancer, especially in triple-negative subtype. Gene Set Enrichment Analysis suggests that miR-20a expression negatively correlates with the autophagy/lysosome pathway. We report here that miR-20a inhibits the basal and nutrient starvation-induced autophagic flux and lysosomal proteolytic activity, increases intracellular reactive oxygen species levels and DNA damage response by targeting several key regulators of autophagy, including BECN1, ATG16L1 and SQSTM1. Re-introduction of exogenous BECN1, ATG16L1 or SQSTM1 reverses the inhibitory effect of miR-20a on autophagy and decreases DNA damage. A negative correlation between miR-20a and its target genes is observed in breast cancer tissues. Lower levels of BECN1, ATG16L1 and SQSTM1 are more common in triple-negative cancers than in other subtypes. High levels of miR-20a also associate with higher frequency of copy-number alterations and DNA mutations in breast cancer patients. Further studies in a xenograft mouse model show that miR-20a promotes tumor initiation and tumor growth. Collectively, these findings suggest that miR-20a-mediated autophagy defect might be a new mechanism underlying the oncogenic function of miRNA during breast tumorigenesis.

Indexed as

AutophagyDNA DamageGenomic InstabilityAnimalsAutophagy-Related ProteinsBeclin-1Biomarkers, TumorBreast NeoplasmsCell Transformation, NeoplasticFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsATG16L1 protein, humanAutophagy-Related ProteinsBeclin-1BECN1 protein, humanBiomarkers, TumorMicroRNAsMIRN20a microRNA, humanSequestosome-1 ProteinSQSTM1 protein, human

Identifiers

PMID28628113
PMCPMC5658668
OpenAlexW2648193553

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.