Evidence map›Paper›PMID 32193335›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2020

Transcriptional suppression of AMPKα1 promotes breast cancer metastasis upon oncogene activation.

Yong Yi, Deshi Chen, Juan Ao, Wenhua Zhang, Jianqiao Yi, Xiaokun Ren, Junjie Fei, Fengtian Li, Mengmeng Niu, Hu Chen and 3 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.6field-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

42 citing papers in PubMed, 80 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Yong YiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.ORCID 0000-0003-4664-9692
Deshi ChenCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Juan AoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Wenhua ZhangCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Jianqiao YiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Xiaokun RenCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Junjie FeiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Fengtian LiCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Mengmeng NiuCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Hu ChenCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Yangkun LuoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China.
Zhijun LuoDepartment of Biochemistry, Boston University School of Medicine, Boston, MA 02118.
Zhi-Xiong Jim XiaoCenter of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences and State Key Laboratory of Biotherapy, Sichuan University, 610064 Chengdu, China; jimzx@scu.edu.cn.ORCID 0000-0003-2504-5742
Sichuan University · CNBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) functions as an energy sensor and is pivotal in maintaining cellular metabolic homeostasis. Numerous studies have shown that down-regulation of AMPK kinase activity or protein stability not only lead to abnormality of metabolism but also contribute to tumor development. However, whether transcription regulation of AMPK plays a critical role in cancer metastasis remains unknown. In this study, we demonstrate that AMPKα1 expression is down-regulated in advanced human breast cancer and is associated with poor clinical outcomes. Transcription of AMPKα1 is inhibited on activation of PI3K and HER2 through ΔNp63α. Ablation of AMPKα1 expression or inhibition of AMPK kinase activity leads to disruption of E-cadherin-mediated cell-cell adhesion in vitro and increased tumor metastasis in vivo. Furthermore, restoration of AMPKα1 expression significantly rescues PI3K/HER2-induced disruption of cell-cell adhesion, cell invasion, and cancer metastasis. Together, these results demonstrate that the transcription control is another layer of AMPK regulation and suggest a critical role for AMPK in regulating cell-cell adhesion and cancer metastasis.

Indexed as

Gene Expression Regulation, NeoplasticAMP-Activated Protein KinasesAnimalsBreastBreast NeoplasmsCell AdhesionCell Line, TumorChromonesDisease-Free SurvivalDown-RegulationErb-b2 Receptor Tyrosine KinasesFemaleGene Knockdown TechniquesHumansLapatinibMice2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAMP-Activated Protein KinasesChromonesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesLapatinibMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPRKAA1 protein, humanTP63 protein, humanTranscription FactorsTumor Suppressor ProteinsAMPKcancer metastasiscell adhesiononcogenic signalingΔNp63α

Identifiers

PMID32193335
PMCPMC7148563
OpenAlexW3011991630

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.