Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway

Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking o...
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Gespeichert in:

Autor*in:	Hichem Bouguerra [verfasserIn] Gorrab Amal [verfasserIn] Stephan Clavel [verfasserIn] Hamouda Boussen [verfasserIn] Jean-François Louet [verfasserIn] Asma Gati [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	leptin breast cancer pgc-1α tumor immune escape β oxidation

Übergeordnetes Werk:	In: Endocrine Connections - Bioscientifica, 2013, 9(2020), 6, Seite 578-586
Übergeordnetes Werk:	volume:9 ; year:2020 ; number:6 ; pages:578-586

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

Katalog-ID:	DOAJ077077040

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allfields	(DE-627)DOAJ077077040 (DE-599)DOAJ835d3c69074647f498dad603a503b83e DE-627 ger DE-627 rakwb eng RC648-665 Hichem Bouguerra verfasserin aut Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients. leptin breast cancer pgc-1α tumor immune escape β oxidation Diseases of the endocrine glands. Clinical endocrinology Gorrab Amal verfasserin aut Stephan Clavel verfasserin aut Hamouda Boussen verfasserin aut Jean-François Louet verfasserin aut Asma Gati verfasserin aut In Endocrine Connections Bioscientifica, 2013 9(2020), 6, Seite 578-586 (DE-627)718731077 (DE-600)2668428-7 20493614 nnns volume:9 year:2020 number:6 pages:578-586 https://doi.org/10.1530/EC-20-0109 kostenfrei https://doaj.org/article/835d3c69074647f498dad603a503b83e kostenfrei https://ec.bioscientifica.com/view/journals/ec/9/6/EC-20-0109.xml kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2020 6 578-586
spelling	(DE-627)DOAJ077077040 (DE-599)DOAJ835d3c69074647f498dad603a503b83e DE-627 ger DE-627 rakwb eng RC648-665 Hichem Bouguerra verfasserin aut Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients. leptin breast cancer pgc-1α tumor immune escape β oxidation Diseases of the endocrine glands. Clinical endocrinology Gorrab Amal verfasserin aut Stephan Clavel verfasserin aut Hamouda Boussen verfasserin aut Jean-François Louet verfasserin aut Asma Gati verfasserin aut In Endocrine Connections Bioscientifica, 2013 9(2020), 6, Seite 578-586 (DE-627)718731077 (DE-600)2668428-7 20493614 nnns volume:9 year:2020 number:6 pages:578-586 https://doi.org/10.1530/EC-20-0109 kostenfrei https://doaj.org/article/835d3c69074647f498dad603a503b83e kostenfrei https://ec.bioscientifica.com/view/journals/ec/9/6/EC-20-0109.xml kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2020 6 578-586
allfields_unstemmed	(DE-627)DOAJ077077040 (DE-599)DOAJ835d3c69074647f498dad603a503b83e DE-627 ger DE-627 rakwb eng RC648-665 Hichem Bouguerra verfasserin aut Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients. leptin breast cancer pgc-1α tumor immune escape β oxidation Diseases of the endocrine glands. Clinical endocrinology Gorrab Amal verfasserin aut Stephan Clavel verfasserin aut Hamouda Boussen verfasserin aut Jean-François Louet verfasserin aut Asma Gati verfasserin aut In Endocrine Connections Bioscientifica, 2013 9(2020), 6, Seite 578-586 (DE-627)718731077 (DE-600)2668428-7 20493614 nnns volume:9 year:2020 number:6 pages:578-586 https://doi.org/10.1530/EC-20-0109 kostenfrei https://doaj.org/article/835d3c69074647f498dad603a503b83e kostenfrei https://ec.bioscientifica.com/view/journals/ec/9/6/EC-20-0109.xml kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2020 6 578-586
allfieldsGer	(DE-627)DOAJ077077040 (DE-599)DOAJ835d3c69074647f498dad603a503b83e DE-627 ger DE-627 rakwb eng RC648-665 Hichem Bouguerra verfasserin aut Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients. leptin breast cancer pgc-1α tumor immune escape β oxidation Diseases of the endocrine glands. Clinical endocrinology Gorrab Amal verfasserin aut Stephan Clavel verfasserin aut Hamouda Boussen verfasserin aut Jean-François Louet verfasserin aut Asma Gati verfasserin aut In Endocrine Connections Bioscientifica, 2013 9(2020), 6, Seite 578-586 (DE-627)718731077 (DE-600)2668428-7 20493614 nnns volume:9 year:2020 number:6 pages:578-586 https://doi.org/10.1530/EC-20-0109 kostenfrei https://doaj.org/article/835d3c69074647f498dad603a503b83e kostenfrei https://ec.bioscientifica.com/view/journals/ec/9/6/EC-20-0109.xml kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2020 6 578-586
allfieldsSound	(DE-627)DOAJ077077040 (DE-599)DOAJ835d3c69074647f498dad603a503b83e DE-627 ger DE-627 rakwb eng RC648-665 Hichem Bouguerra verfasserin aut Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients. leptin breast cancer pgc-1α tumor immune escape β oxidation Diseases of the endocrine glands. Clinical endocrinology Gorrab Amal verfasserin aut Stephan Clavel verfasserin aut Hamouda Boussen verfasserin aut Jean-François Louet verfasserin aut Asma Gati verfasserin aut In Endocrine Connections Bioscientifica, 2013 9(2020), 6, Seite 578-586 (DE-627)718731077 (DE-600)2668428-7 20493614 nnns volume:9 year:2020 number:6 pages:578-586 https://doi.org/10.1530/EC-20-0109 kostenfrei https://doaj.org/article/835d3c69074647f498dad603a503b83e kostenfrei https://ec.bioscientifica.com/view/journals/ec/9/6/EC-20-0109.xml kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei https://doaj.org/toc/2049-3614 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2020 6 578-586
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source	In Endocrine Connections 9(2020), 6, Seite 578-586 volume:9 year:2020 number:6 pages:578-586
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authorswithroles_txt_mv	Hichem Bouguerra @@aut@@ Gorrab Amal @@aut@@ Stephan Clavel @@aut@@ Hamouda Boussen @@aut@@ Jean-François Louet @@aut@@ Asma Gati @@aut@@
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callnumber-first	R - Medicine
author	Hichem Bouguerra
spellingShingle	Hichem Bouguerra misc RC648-665 misc leptin misc breast cancer misc pgc-1α misc tumor immune escape misc β oxidation misc Diseases of the endocrine glands. Clinical endocrinology Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway
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topic_title	RC648-665 Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway leptin breast cancer pgc-1α tumor immune escape β oxidation
topic	misc RC648-665 misc leptin misc breast cancer misc pgc-1α misc tumor immune escape misc β oxidation misc Diseases of the endocrine glands. Clinical endocrinology
topic_unstemmed	misc RC648-665 misc leptin misc breast cancer misc pgc-1α misc tumor immune escape misc β oxidation misc Diseases of the endocrine glands. Clinical endocrinology
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title	Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway
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title_full	Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway
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title_sort	leptin decreases bc cell susceptibility to nk lysis via pgc1a pathway
callnumber	RC648-665
title_auth	Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway
abstract	Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients.
abstractGer	Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients.
abstract_unstemmed	Large prospective studies established a link between obesity and breast cancer (BC) development. Yet, the mechanisms underlying this association are not fully understood. Among the diverse adipocytokine secreted by hypertrophic adipose tissue, leptin is emerging as a key candidate molecule linking obesity and cancer, since it promotes proliferation and invasiveness of tumors. However, the potential implication of leptin on tumor escape mechanisms remains unknown. This study aims to explore the effect of leptin on tumor resistance to NK lysis and the underlying mechanism. We found that leptin promotes both BC resistance to NK92-mediated lysis and β oxidation on MCF-7, by the up-regulation of a master regulator of mitochondrial biogenesis, the peroxisome proliferator activated receptor coactivator-1 α (PGC1A). Using adenoviral approaches, we show that acute elevation of PGC1A enhances the fatty acid oxidation pathway and decreases the susceptibility of BC cells to NK92-mediated lysis . Importantly, we identified the involvement of PGC1A and leptin in the regulation of hypoxia inducible factor-1 alpha (HIF1A) expression by tumor cells. We further demonstrate that basal BC cells MDA-MB-231 and BT-20 exhibit an increased PGC1A mRNA level and an enhanced oxidative phosphorylation activity; in comparison with luminal BC cells MCF7 and MDA-361, which are associated with more resistance NK92 lysis. Altogether, our results demonstrate for the first time how leptin could promote tumor resistance to immu ne attacks. Reagents blocking leptin or PGC1A activity might aid in developing new therapeutic strategies to limit tumor development in obese BC patients.
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title_short	Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway
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Leptin decreases BC cell susceptibility to NK lysis via PGC1A pathway

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