GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells

Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to t...
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Autor*in:	Naiara Santana-Codina [verfasserIn] Anna Marcé-Grau [verfasserIn] Laia Muixí [verfasserIn] Claudia Nieva [verfasserIn] Mónica Marro [verfasserIn] David Sebastián [verfasserIn] Juan Pablo Muñoz [verfasserIn] Antonio Zorzano [verfasserIn] Angels Sierra [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	GRP94 brain metastasis endoplasmic reticulum stress fatty acids

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 20(2019), 16, p 3883
Übergeordnetes Werk:	volume:20 ; year:2019 ; number:16, p 3883

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/ijms20163883

Katalog-ID:	DOAJ003916928

Internformat


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allfields	10.3390/ijms20163883 doi (DE-627)DOAJ003916928 (DE-599)DOAJ5a0073dd23d944758dad0f5ee90f6134 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Naiara Santana-Codina verfasserin aut GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression. GRP94 brain metastasis endoplasmic reticulum stress fatty acids Biology (General) Chemistry Anna Marcé-Grau verfasserin aut Laia Muixí verfasserin aut Claudia Nieva verfasserin aut Mónica Marro verfasserin aut David Sebastián verfasserin aut Juan Pablo Muñoz verfasserin aut Antonio Zorzano verfasserin aut Angels Sierra verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 16, p 3883 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:16, p 3883 https://doi.org/10.3390/ijms20163883 kostenfrei https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 kostenfrei https://www.mdpi.com/1422-0067/20/16/3883 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_70 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 20 2019 16, p 3883
spelling	10.3390/ijms20163883 doi (DE-627)DOAJ003916928 (DE-599)DOAJ5a0073dd23d944758dad0f5ee90f6134 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Naiara Santana-Codina verfasserin aut GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression. GRP94 brain metastasis endoplasmic reticulum stress fatty acids Biology (General) Chemistry Anna Marcé-Grau verfasserin aut Laia Muixí verfasserin aut Claudia Nieva verfasserin aut Mónica Marro verfasserin aut David Sebastián verfasserin aut Juan Pablo Muñoz verfasserin aut Antonio Zorzano verfasserin aut Angels Sierra verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 16, p 3883 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:16, p 3883 https://doi.org/10.3390/ijms20163883 kostenfrei https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 kostenfrei https://www.mdpi.com/1422-0067/20/16/3883 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_70 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 20 2019 16, p 3883
allfields_unstemmed	10.3390/ijms20163883 doi (DE-627)DOAJ003916928 (DE-599)DOAJ5a0073dd23d944758dad0f5ee90f6134 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Naiara Santana-Codina verfasserin aut GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression. GRP94 brain metastasis endoplasmic reticulum stress fatty acids Biology (General) Chemistry Anna Marcé-Grau verfasserin aut Laia Muixí verfasserin aut Claudia Nieva verfasserin aut Mónica Marro verfasserin aut David Sebastián verfasserin aut Juan Pablo Muñoz verfasserin aut Antonio Zorzano verfasserin aut Angels Sierra verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 16, p 3883 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:16, p 3883 https://doi.org/10.3390/ijms20163883 kostenfrei https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 kostenfrei https://www.mdpi.com/1422-0067/20/16/3883 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_70 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 20 2019 16, p 3883
allfieldsGer	10.3390/ijms20163883 doi (DE-627)DOAJ003916928 (DE-599)DOAJ5a0073dd23d944758dad0f5ee90f6134 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Naiara Santana-Codina verfasserin aut GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression. GRP94 brain metastasis endoplasmic reticulum stress fatty acids Biology (General) Chemistry Anna Marcé-Grau verfasserin aut Laia Muixí verfasserin aut Claudia Nieva verfasserin aut Mónica Marro verfasserin aut David Sebastián verfasserin aut Juan Pablo Muñoz verfasserin aut Antonio Zorzano verfasserin aut Angels Sierra verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 16, p 3883 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:16, p 3883 https://doi.org/10.3390/ijms20163883 kostenfrei https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 kostenfrei https://www.mdpi.com/1422-0067/20/16/3883 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_70 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 20 2019 16, p 3883
allfieldsSound	10.3390/ijms20163883 doi (DE-627)DOAJ003916928 (DE-599)DOAJ5a0073dd23d944758dad0f5ee90f6134 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Naiara Santana-Codina verfasserin aut GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression. GRP94 brain metastasis endoplasmic reticulum stress fatty acids Biology (General) Chemistry Anna Marcé-Grau verfasserin aut Laia Muixí verfasserin aut Claudia Nieva verfasserin aut Mónica Marro verfasserin aut David Sebastián verfasserin aut Juan Pablo Muñoz verfasserin aut Antonio Zorzano verfasserin aut Angels Sierra verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 20(2019), 16, p 3883 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:20 year:2019 number:16, p 3883 https://doi.org/10.3390/ijms20163883 kostenfrei https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 kostenfrei https://www.mdpi.com/1422-0067/20/16/3883 kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_70 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_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 20 2019 16, p 3883
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source	In International Journal of Molecular Sciences 20(2019), 16, p 3883 volume:20 year:2019 number:16, p 3883
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callnumber-first	Q - Science
author	Naiara Santana-Codina
spellingShingle	Naiara Santana-Codina misc QH301-705.5 misc QD1-999 misc GRP94 misc brain metastasis misc endoplasmic reticulum stress misc fatty acids misc Biology (General) misc Chemistry GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells
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topic_title	QH301-705.5 QD1-999 GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells GRP94 brain metastasis endoplasmic reticulum stress fatty acids
topic	misc QH301-705.5 misc QD1-999 misc GRP94 misc brain metastasis misc endoplasmic reticulum stress misc fatty acids misc Biology (General) misc Chemistry
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title	GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells
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title_full	GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells
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title_sort	grp94 is involved in the lipid phenotype of brain metastatic cells
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title_auth	GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells
abstract	Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression.
abstractGer	Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression.
abstract_unstemmed	Metabolic adaptation may happen in response to the pressure exerted by the microenvironment and is a key step in survival of metastatic cells. Brain metastasis occurs as a consequence of the systemic dissemination of tumor cells, a fact that correlates with poor prognosis and high morbidity due to the difficulty in identifying biomarkers that allow a more targeted therapy. Previously, we performed transcriptomic analysis of human breast cancer patient samples and evaluated the differential expression of genes in brain metastasis (BrM) compared to lung, bone and liver metastasis. Our network approach identified upregulation of glucose-regulated protein 94 (GRP94) as well as proteins related to synthesis of fatty acids (FA) in BrM. Here we report that BrM cells show an increase in FA content and decreased saturation with regard to parental cells measured by Raman spectroscopy that differentiate BrM from other metastases. Moreover, BrM cells exerted a high ability to oxidize FA and compensate hypoglycemic stress due to an overexpression of proteins involved in FA synthesis and degradation (SREBP-1, LXRα, ACOT7). GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. In conclusion, GRP94 is required for the metabolic stress survival of BrM cells, and it might act as a modulator of lipid metabolism to favor BrM progression.
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title_short	GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells
url	https://doi.org/10.3390/ijms20163883 https://doaj.org/article/5a0073dd23d944758dad0f5ee90f6134 https://www.mdpi.com/1422-0067/20/16/3883 https://doaj.org/toc/1422-0067
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author2	Anna Marcé-Grau Laia Muixí Claudia Nieva Mónica Marro David Sebastián Juan Pablo Muñoz Antonio Zorzano Angels Sierra
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up_date	2024-07-03T20:52:47.478Z
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GRP94 ablation restored glucose dependence, down-regulated ACOT7 and SREBP-1 and decreased tumorigenicity in vivo. 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GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells

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