Evidence map›Paper›PMID 27977328›Full record

ArticleAutophagy2017

Transcriptional regulation of core autophagy and lysosomal genes by the androgen receptor promotes prostate cancer progression.

Alicia M Blessing, Kimal Rajapakshe, Lakshmi Reddy Bollu, Yan Shi, Mark A White, Alexander H Pham, Chenchu Lin, Philip Jonsson, Constanza J Cortes, Edwin Cheung and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 116 citations in OpenAlex.

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15 more citing papers are in PubMed but not listed here.

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

15 authors at 7 institutions in 2 countries.

Alicia M Blessinga Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Kimal Rajapakshec Department of Molecular and Cellular Biology , Baylor College of Medicine , Houston , TX , USA.
Lakshmi Reddy Bollud Department of Clinical Cancer Prevention , The University of Texas M.D. Anderson Cancer Center , Houston , TX , USA.
Yan Shia Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Mark A Whitea Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Alexander H Phama Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Chenchu Lina Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Philip Jonssona Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
Constanza J Cortese Departments of Cellular and Molecular Medicine , Neurosciences, and Pediatrics, Division of Biological Sciences, Institute for Genomic Medicine, Sanford Consortium for Regenerative Medicine, University of California , San Diego, La Jolla , CA , USA.
Edwin Cheungf Faculty of Health Sciences, University of Macau , Taipa , Macau , China.
Albert R La Spadae Departments of Cellular and Molecular Medicine , Neurosciences, and Pediatrics, Division of Biological Sciences, Institute for Genomic Medicine, Sanford Consortium for Regenerative Medicine, University of California , San Diego, La Jolla , CA , USA.
Robert C Bastb Department of Experimental Therapeutics , The University of Texas M.D. Anderson Cancer Center , Houston , TX , USA.
Fatima A Merchantg Department of Engineering Technology , University of Houston , Houston , TX , USA.
Cristian Coarfac Department of Molecular and Cellular Biology , Baylor College of Medicine , Houston , TX , USA.
Daniel E Frigoa Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry , University of Houston , Houston , TX , USA.
University of Houston · USThe University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USHouston Methodist · USSanford Consortium for Regenerative Medicine · USUniversity of California, San Diego · USUniversity of Macau · MO

Funding

Molecular genetic regulation of autophagy in health and neurodegenerative diseaseR01AG033082 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2009 to 2019
$4.0M
Deconstructing the cellular and molecular basis of SBMA motor neuron disease: From mechanism to therapyR01NS100023 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LA SPADA, ALBERT R · 2016 to 2020
$2.4M
Genetic & Metabolic Dissection of the CaMKKbeta Signaling Axis in Prostate CancerR01CA184208 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FRIGO, DANIEL EDWARD · 2015 to 2019
$1.9M
Androgenic Regulation of Autophagy in the ProstateR03DK092434 · NIDDK · UNIVERSITY OF HOUSTON · PI FRIGO, DANIEL EDWARD · 2011 to 2012
$150k
NCI NIH HHS R01 CA184208NIA NIH HHS R01 AG033082NIDDK NIH HHS R03 DK092434NINDS NIH HHS R01 NS100023
6 · The paper itself

Abstract

AR (androgen receptor) signaling is crucial for the development and maintenance of the prostate as well as the initiation and progression of prostate cancer. Despite the AR's central role in prostate cancer progression, it is still unclear which AR-mediated processes drive the disease. Here, we identified 4 core autophagy genes: ATG4B, ATG4D, ULK1, and ULK2, in addition to the transcription factor TFEB, a master regulator of lysosomal biogenesis and function, as transcriptional targets of AR in prostate cancer. These findings were significant in light of our recent observation that androgens promoted prostate cancer cell growth in part through the induction of autophagy. Expression of these 5 genes was essential for maximal androgen-mediated autophagy and cell proliferation. In addition, expression of each of these 5 genes alone or in combination was sufficient to increase prostate cancer cell growth independent of AR activity. Further, bioinformatic analysis demonstrated that the expression of these genes correlated with disease progression in 3 separate clinical cohorts. Collectively, these findings demonstrate a functional role for increased autophagy in prostate cancer progression, provide a mechanism for how autophagy is augmented, and highlight the potential of targeting this process for the treatment of advanced prostate cancer.

Indexed as

Disease ProgressionGene Expression Regulation, NeoplasticTranscription, GeneticAndrogensAutophagyAutophagy-Related ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Line, TumorCell ProliferationGene Expression ProfilingHEK293 CellsHumansLysosomesMaleNeoplasm MetastasisPrognosisAndrogensAR protein, humanAutophagy-Related ProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsReceptors, AndrogenTFEB protein, humanandrogenandrogen receptor (AR)ATG4BATG4Dautophagynuclear receptorprostate cancerTFEBULK1ULK2

Identifiers

PMID27977328
PMCPMC5361609
OpenAlexW2567547124

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.