Evidence map›Paper›PMID 25811979›Full record

ArticlePloS one2015

YAP enhances autophagic flux to promote breast cancer cell survival in response to nutrient deprivation.

Qinghe Song, Beibei Mao, Jinbo Cheng, Yuhao Gao, Ke Jiang, Jun Chen, Zengqiang Yuan, Songshu Meng

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 70 citations in OpenAlex.

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  15. Review
  16. Context-dependent roles of YAP/TAZ in stem cell fates and cancer.Cellular and molecular life sciences : CMLS · 2021
    Review
  17. YAP promotes autophagy and progression of gliomas via upregulating HMGB1.Journal of experimental & clinical cancer research : CR · 2021
    Article
  18. 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

8 authors at 5 institutions in 1 country.

Qinghe SongState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
Beibei MaoState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Jinbo ChengState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Yuhao GaoState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
Ke JiangInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, Dalian, Liaoning, China.
Jun ChenCenter of Growth, Metabolism and Aging, College of Life Sciences, Sichuan University, Chengdu, China.
Zengqiang YuanState Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
Songshu MengInstitute of Cancer Stem Cell, Dalian Medical University Cancer Center, Dalian, Liaoning, China.
Chinese Academy of Sciences · CNDalian Medical University · CNUniversity of Chinese Academy of Sciences · CNInstitute of Biophysics · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Yes-associated protein (YAP), a transcriptional coactivator inactivated by the Hippo tumor suppressor pathway, functions as an oncoprotein in a variety of cancers. However, its contribution to breast cancer remains controversial. This study investigated the role of YAP in breast cancer cells under nutrient deprivation (ND). Here, we show that YAP knockdown sensitized MCF7 breast cancer cells to nutrient deprivation-induced apoptosis. Furthermore, in response to ND, YAP increased the autolysosome degradation, thereby enhancing the cellular autophagic flux in breast cancer cells. Of note, autophagy is crucial for YAP to protect MCF7 cells from apoptosis under ND conditions. In addition, the TEA domain (TEAD) family of growth-promoting transcription factors was indispensable for YAP-mediated regulation of autophagy. Collectively, our data reveal a role for YAP in promoting breast cancer cell survival upon ND stress and uncover an unappreciated function of YAP/TEAD in the regulation of autophagy.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisAutophagyBreast NeoplasmsCell Line, TumorCell SurvivalFemaleGene Knockdown TechniquesHumansLysosomesMCF-7 CellsPhosphoproteinsProtein BindingTranscription FactorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingPhosphoproteinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID25811979
PMCPMC4374846
OpenAlexW2091718668

What OpenQuestion holds

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LicenceCC BY
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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.