ChloroquineV1, Istex, Corpus, bibRecord, 001073

Mitophagy defects arising from BNip3 loss promote mammary tumor progression to metastasis

Identifieur interne : 001073 ( Istex/Corpus ); précédent : 001072; suivant : 001074

Mitophagy defects arising from BNip3 loss promote mammary tumor progression to metastasis

Auteurs : Aparajita H. Chourasia ; Kristin Tracy ; Casey Frankenberger ; Michelle L. Boland ; Marina N. Sharifi ; Lauren E. Drake ; Joseph R. Sachleben ; John M. Asara ; Jason W. Locasale ; Gregory S. Karczmar ; Kay F. Macleod

Source :

EMBO reports [ 1469-221X ] ; 2015-09.

RBID : ISTEX:889AC4239FEC187EECBBCA568014D874C3FAAA01

Abstract

BNip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for BNip3 in a clinically relevant mouse model of mammary tumorigenesis. BNip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess ROS production. In the absence of BNip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial ROS increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in BNip3‐null tumors. Glycolysis inhibition attenuates the growth of BNip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that BNIP3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (TNBC). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying TNBC for treatment.

This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer. Elevated ROS production by dysfunctional mitochondria in BNip3 null tumors results in increased Hif‐1α levels and increased tumor progression to invasiveness. This novel negative feedback loop between BNip3 and Hif‐1α limits the oncogenic activity of Hif‐1 in glycolysis and angiogenesis. Defective mitochondria and aerobic glycolysis arising from loss of BNip3 is associated with increased dependence on autophagy for survival. BNIP3 is focally deleted in triple negative breast cancer and, together with high HIF‐1α levels, strongly predicts progression to metastasis in TNBC patients.

Url:

https://api.istex.fr/ark:/67375/WNG-42LNK323-C/fulltext.pdf

DOI: 10.15252/embr.201540759

Links to Exploration step

ISTEX:889AC4239FEC187EECBBCA568014D874C3FAAA01

Le document en format XML

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<front><div type="abstract">BNip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for BNip3 in a clinically relevant mouse model of mammary tumorigenesis. BNip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess ROS production. In the absence of BNip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial ROS increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in BNip3‐null tumors. Glycolysis inhibition attenuates the growth of BNip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that BNIP3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (TNBC). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying TNBC for treatment.</div>
<div type="abstract">This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer. Elevated ROS production by dysfunctional mitochondria in BNip3 null tumors results in increased Hif‐1α levels and increased tumor progression to invasiveness. This novel negative feedback loop between BNip3 and Hif‐1α limits the oncogenic activity of Hif‐1 in glycolysis and angiogenesis. Defective mitochondria and aerobic glycolysis arising from loss of BNip3 is associated with increased dependence on autophagy for survival. BNIP3 is focally deleted in triple negative breast cancer and, together with high HIF‐1α levels, strongly predicts progression to metastasis in TNBC patients.</div>
<div type="abstract">This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.</div>
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<abstract>BNip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for BNip3 in a clinically relevant mouse model of mammary tumorigenesis. BNip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess ROS production. In the absence of BNip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial ROS increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in BNip3‐null tumors. Glycolysis inhibition attenuates the growth of BNip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that BNIP3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (TNBC). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying TNBC for treatment.</abstract>
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<profileDesc><abstract style="main" xml:id="embr201540759-abs-0001"><head>Abstract</head>
<p><hi rend="fc">BN</hi>
ip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for <hi rend="fc">BN</hi>
ip3 in a clinically relevant mouse model of mammary tumorigenesis. <hi rend="fc">BN</hi>
ip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess <hi rend="fc">ROS</hi>
 production. In the absence of <hi rend="fc">BN</hi>
ip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial <hi rend="fc">ROS</hi>
 increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in <hi rend="fc">BN</hi>
ip3‐null tumors. Glycolysis inhibition attenuates the growth of <hi rend="fc">BN</hi>
ip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that <hi rend="fc">BNIP</hi>
3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (<hi rend="fc">TNBC</hi>
). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying <hi rend="fc">TNBC</hi>
 for treatment.</p>
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<p>This study shows that <hi rend="fc">BN</hi>
ip3 loss and the ensuing defects in mitophagy lead to <hi rend="fc">ROS</hi>
 production, Hif transcriptional responses and mammary tumor progression. <hi rend="fc">BNIP</hi>
3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.</p>
<p><list xml:id="embr201540759-list-0001" style="bulleted"><item>Elevated ROS production by dysfunctional mitochondria in BNip3 null tumors results in increased Hif‐1α levels and increased tumor progression to invasiveness.</item>
<item>This novel negative feedback loop between BNip3 and Hif‐1α limits the oncogenic activity of Hif‐1 in glycolysis and angiogenesis.</item>
<item>Defective mitochondria and aerobic glycolysis arising from loss of BNip3 is associated with increased dependence on autophagy for survival.</item>
<item>BNIP3 is focally deleted in triple negative breast cancer and, together with high HIF‐1α levels, strongly predicts progression to metastasis in TNBC patients.</item>
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<abstract style="graphical" xml:id="embr201540759-abs-0003"><p>This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.
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<term xml:id="embr201540759-kwd-0002">breast cancer</term>
<term xml:id="embr201540759-kwd-0003">glycolysis</term>
<term xml:id="embr201540759-kwd-0004"><hi rend="fc">HIF</hi>
‐1α</term>
<term xml:id="embr201540759-kwd-0005">invasive carcinoma</term>
<term xml:id="embr201540759-kwd-0006">mitophagy</term>
<term xml:id="embr201540759-kwd-0007"><hi rend="fc">ROS</hi>
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<textClass><keywords ana="subject"><term ref="http://psi.embo.org/14693178/EMBO07">Autophagy & Cell Death</term>
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<correspondenceTo>Corresponding author. Tel: +1 773 834 8309; Fax: +1 773 702 4476; E‐mail: <email>kmacleod@uchicago.edu</email>
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 <orgName>Cornell University</orgName>
 <address><city>Ithaca</city>
 <countryPart>NY</countryPart>
 <country>USA</country>
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<affiliation countryCode="US" type="organization" xml:id="embr201540759-aff-0008"><orgDiv>Department of Radiology</orgDiv>
 <orgName>The University of Chicago</orgName>
 <address><city>Chicago</city>
 <countryPart>IL</countryPart>
 <country>USA</country>
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<keywordGroup type="author"><keyword xml:id="embr201540759-kwd-0001"><fc>BN</fc>
ip3</keyword>
<keyword xml:id="embr201540759-kwd-0002">breast cancer</keyword>
<keyword xml:id="embr201540759-kwd-0003">glycolysis</keyword>
<keyword xml:id="embr201540759-kwd-0004"><fc>HIF</fc>
‐1α</keyword>
<keyword xml:id="embr201540759-kwd-0005">invasive carcinoma</keyword>
<keyword xml:id="embr201540759-kwd-0006">mitophagy</keyword>
<keyword xml:id="embr201540759-kwd-0007"><fc>ROS</fc>
</keyword>
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<fundingNumber>RO1 CA131188</fundingNumber>
<fundingNumber>RO1 CA162405</fundingNumber>
<fundingNumber>T32 CA009594</fundingNumber>
<fundingNumber>T32 DK780073</fundingNumber>
<fundingNumber>RO1 CA133490</fundingNumber>
</fundingInfo>
<fundingInfo><fundingAgency>University of Chicago Medical Scientist Training Program</fundingAgency>
</fundingInfo>
<fundingInfo><fundingAgency>Human Tissue Resource Center</fundingAgency>
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<fundingInfo><fundingAgency>University of Chicago Cancer Center</fundingAgency>
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<abstractGroup><abstract type="main" xml:id="embr201540759-abs-0001"><title type="main">Abstract</title>
<p><fc>BN</fc>
ip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for <fc>BN</fc>
ip3 in a clinically relevant mouse model of mammary tumorigenesis. <fc>BN</fc>
ip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess <fc>ROS</fc>
 production. In the absence of <fc>BN</fc>
ip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial <fc>ROS</fc>
 increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in <fc>BN</fc>
ip3‐null tumors. Glycolysis inhibition attenuates the growth of <fc>BN</fc>
ip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that <fc>BNIP</fc>
3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (<fc>TNBC</fc>
). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying <fc>TNBC</fc>
 for treatment.</p>
</abstract>
<abstract type="synopsis" xml:id="embr201540759-abs-0002"><title type="main">Synopsis</title>
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<p>This study shows that <fc>BN</fc>
ip3 loss and the ensuing defects in mitophagy lead to <fc>ROS</fc>
 production, Hif transcriptional responses and mammary tumor progression. <fc>BNIP</fc>
3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.</p>
<p><list formatted="paragraph" style="bulleted" xml:id="embr201540759-list-0001"><listItem>Elevated ROS production by dysfunctional mitochondria in BNip3 null tumors results in increased Hif‐1α levels and increased tumor progression to invasiveness.</listItem>
<listItem>This novel negative feedback loop between BNip3 and Hif‐1α limits the oncogenic activity of Hif‐1 in glycolysis and angiogenesis.</listItem>
<listItem>Defective mitochondria and aerobic glycolysis arising from loss of BNip3 is associated with increased dependence on autophagy for survival.</listItem>
<listItem>BNIP3 is focally deleted in triple negative breast cancer and, together with high HIF‐1α levels, strongly predicts progression to metastasis in TNBC patients.</listItem>
</list>
</p>
</abstract>
<abstract type="graphical" xml:id="embr201540759-abs-0003"><p>This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.
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<name type="personal"><namePart type="given">Aparajita H</namePart>
<namePart type="family">Chourasia</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA</affiliation>
<affiliation>The Committee on Cancer Biology, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Kristin</namePart>
<namePart type="family">Tracy</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA</affiliation>
<affiliation>The Committee on Cancer Biology, IL, Chicago, USA</affiliation>
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<name type="personal"><namePart type="given">Casey</namePart>
<namePart type="family">Frankenberger</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Michelle L</namePart>
<namePart type="family">Boland</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA</affiliation>
<affiliation>The Committee on Molecular Metabolism and Nutrition, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Marina N</namePart>
<namePart type="family">Sharifi</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA</affiliation>
<affiliation>The Committee on Cancer Biology, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Lauren E</namePart>
<namePart type="family">Drake</namePart>
<affiliation>The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL, USA</affiliation>
<affiliation>The Committee on Molecular Pathogenesis & Molecular Medicine, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Joseph R</namePart>
<namePart type="family">Sachleben</namePart>
<affiliation>Biomolecular NMR Facility, The University of Chicago, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">John M</namePart>
<namePart type="family">Asara</namePart>
<affiliation>Division of Signal Transduction, Beth Israel Deaconess Medical Center and Harvard Medical School, MA, Boston, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
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<name type="personal"><namePart type="given">Jason W</namePart>
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<affiliation>Division of Nutritional Sciences, Cornell University, NY, Ithaca, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Gregory S</namePart>
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<affiliation>Department of Radiology, The University of Chicago, IL, Chicago, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Kay F</namePart>
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<affiliation>The Committee on Cancer Biology, Chicago, IL, USA</affiliation>
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<abstract>BNip3 is a hypoxia‐inducible protein that targets mitochondria for autophagosomal degradation. We report a novel tumor suppressor role for BNip3 in a clinically relevant mouse model of mammary tumorigenesis. BNip3 delays primary mammary tumor growth and progression by preventing the accumulation of dysfunctional mitochondria and resultant excess ROS production. In the absence of BNip3, mammary tumor cells are unable to reduce mitochondrial mass effectively and elevated mitochondrial ROS increases the expression of Hif‐1α and Hif target genes, including those involved in glycolysis and angiogenesis—two processes that are also markedly increased in BNip3‐null tumors. Glycolysis inhibition attenuates the growth of BNip3‐null tumor cells, revealing an increased dependence on autophagy for survival. We also demonstrate that BNIP3 deletion can be used as a prognostic marker of tumor progression to metastasis in human triple‐negative breast cancer (TNBC). These studies show that mitochondrial dysfunction—caused by defects in mitophagy—can promote the Warburg effect and tumor progression, and suggest better approaches to stratifying TNBC for treatment.</abstract>
<abstract type="synopsis">This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer. Elevated ROS production by dysfunctional mitochondria in BNip3 null tumors results in increased Hif‐1α levels and increased tumor progression to invasiveness. This novel negative feedback loop between BNip3 and Hif‐1α limits the oncogenic activity of Hif‐1 in glycolysis and angiogenesis. Defective mitochondria and aerobic glycolysis arising from loss of BNip3 is associated with increased dependence on autophagy for survival. BNIP3 is focally deleted in triple negative breast cancer and, together with high HIF‐1α levels, strongly predicts progression to metastasis in TNBC patients.</abstract>
<abstract type="graphical">This study shows that BNip3 loss and the ensuing defects in mitophagy lead to ROS production, Hif transcriptional responses and mammary tumor progression. BNIP3 deletion is a prognostic marker of metastatic potential in triple negative breast cancer.</abstract>
<note type="additional physical form">Expanded View Figures PDFReview Process File</note>
<note type="funding">NIH - No. RO1 CA131188; No. RO1 CA162405; No. T32 CA009594; No. T32 DK780073; No. RO1 CA133490; </note>
<note type="funding">University of Chicago Medical Scientist Training Program</note>
<note type="funding">Human Tissue Resource Center</note>
<note type="funding">University of Chicago Cancer Center</note>
<subject><genre>keywords</genre>
<topic>BNip3</topic>
<topic>breast cancer</topic>
<topic>glycolysis</topic>
<topic>HIF‐1α</topic>
<topic>invasive carcinoma</topic>
<topic>mitophagy</topic>
<topic>ROS</topic>
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<topic authorityURI="http://psi.embo.org/14693178/EMBO07">Autophagy & Cell Death</topic>
<topic authorityURI="http://psi.embo.org/14693178/EMBO03">Cancer</topic>
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<identifier type="ISSN">1469-221X</identifier>
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Mitophagy defects arising from BNip3 loss promote mammary tumor progression to metastasis

Mitophagy defects arising from BNip3 loss promote mammary tumor progression to metastasis

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