Difference between revisions of "Victorino 2015 Tumour Biol"
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{{Publication | {{Publication | ||
|title=Victorino VJ, Barroso WA, Assunção AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP (2015) PGC-1β regulates HER2-overexpressing breast cancer cells proliferation by metabolic and redox pathways. Tumour Biol | |title=Victorino VJ, Barroso WA, Assunção AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP (2015) PGC-1β regulates HER2-overexpressing breast cancer cells proliferation by metabolic and redox pathways. Tumour Biol 37:6035-44. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26602383 PMID: 26602383] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26602383 PMID: 26602383] | ||
|authors=Victorino VJ, Barroso WA, Assuncao AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP | |authors=Victorino VJ, Barroso WA, Assuncao AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP | ||
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|journal=Tumour Biol | |journal=Tumour Biol | ||
|abstract=Breast cancer is a prevalent neoplastic disease among women worldwide which treatments still present several side effects and resistance. Considering that cancer cells present derangements in their energetic homeostasis, and that peroxisome proliferator-activated receptor- gamma coactivator 1 (PGC-1) is crucial for cellular metabolism and redox signaling, the main objective of this study was to investigate whether there is a relationship between PGC-1 expression, the proliferation of breast cancer cells and the mechanisms involved. We initially assessed PGC-1β expression in complementary DNA (cDNA) from breast tumor of patients bearing luminal A, luminal B, and HER2-overexpressed and triple negative tumors. Our data showed that PGC-1β expression is increased in patients bearing HER2-overexpressing tumors as compared to others subtypes. Using quantitative PCR and immunoblotting, we showed that breast cancer cells with HER2-amplification (SKBR-3) have greater expression of PGC-1β as compared to a non-tumorous breast cell (MCF-10A) and higher proliferation rate. PGC-1β expression was knocked down with short interfering RNA in HER2-overexpressing cells, and cells decreased proliferation. In these PGC-1β-inhibited cells, we found increased citrate synthase activity and no marked changes in mitochondrial respiration. Glycolytic pathway was decreased, characterized by lower intracellular lactate levels. In addition, after PGC-1β knockdown, SKBR-3 cells showed increased reactive oxygen species production, no changes in antioxidant activity, and decreased expression of ERRα, a modulator of metabolism. In conclusion, we show an association of HER2-overexpression and PGC-1β. PGC-1β knockdown impairs HER2-overexpressing cells proliferation acting on ERRα signaling, metabolism, and redox balance. | |abstract=Breast cancer is a prevalent neoplastic disease among women worldwide which treatments still present several side effects and resistance. Considering that cancer cells present derangements in their energetic homeostasis, and that peroxisome proliferator-activated receptor- gamma coactivator 1 (PGC-1) is crucial for cellular metabolism and redox signaling, the main objective of this study was to investigate whether there is a relationship between PGC-1 expression, the proliferation of breast cancer cells and the mechanisms involved. We initially assessed PGC-1β expression in complementary DNA (cDNA) from breast tumor of patients bearing luminal A, luminal B, and HER2-overexpressed and triple negative tumors. Our data showed that PGC-1β expression is increased in patients bearing HER2-overexpressing tumors as compared to others subtypes. Using quantitative PCR and immunoblotting, we showed that breast cancer cells with HER2-amplification (SKBR-3) have greater expression of PGC-1β as compared to a non-tumorous breast cell (MCF-10A) and higher proliferation rate. PGC-1β expression was knocked down with short interfering RNA in HER2-overexpressing cells, and cells decreased proliferation. In these PGC-1β-inhibited cells, we found increased citrate synthase activity and no marked changes in mitochondrial respiration. Glycolytic pathway was decreased, characterized by lower intracellular lactate levels. In addition, after PGC-1β knockdown, SKBR-3 cells showed increased reactive oxygen species production, no changes in antioxidant activity, and decreased expression of ERRα, a modulator of metabolism. In conclusion, we show an association of HER2-overexpression and PGC-1β. PGC-1β knockdown impairs HER2-overexpressing cells proliferation acting on ERRα signaling, metabolism, and redox balance. | ||
|keywords=Breast cancer subtypes, HER2-overexpressing, PGC-1β, Proliferation | |keywords=Breast cancer subtypes, HER2-overexpressing, PGC-1β, Proliferation, Human breast adenocarcinoma SKBR-3 cells | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| | |area=Respiration, Genetic knockout;overexpression, Patients | ||
|diseases=Cancer | |||
|organism=Human | |||
|tissues=Genital, Other cell lines | |||
|preparations=Intact cells | |||
|couplingstates=LEAK, ROUTINE, ET | |||
|pathways=ROX | |||
|instruments=Oxygraph-2k | |||
|additional=2016-01 | |||
}} | }} |
Latest revision as of 16:27, 13 November 2017
Victorino VJ, Barroso WA, Assunção AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP (2015) PGC-1β regulates HER2-overexpressing breast cancer cells proliferation by metabolic and redox pathways. Tumour Biol 37:6035-44. |
Victorino VJ, Barroso WA, Assuncao AK, Cury V, Jeremias IC, Petroni R, Chausse B, Ariga SK, Herrera AC, Panis C, Lima TM, Souza HP (2015) Tumour Biol
Abstract: Breast cancer is a prevalent neoplastic disease among women worldwide which treatments still present several side effects and resistance. Considering that cancer cells present derangements in their energetic homeostasis, and that peroxisome proliferator-activated receptor- gamma coactivator 1 (PGC-1) is crucial for cellular metabolism and redox signaling, the main objective of this study was to investigate whether there is a relationship between PGC-1 expression, the proliferation of breast cancer cells and the mechanisms involved. We initially assessed PGC-1β expression in complementary DNA (cDNA) from breast tumor of patients bearing luminal A, luminal B, and HER2-overexpressed and triple negative tumors. Our data showed that PGC-1β expression is increased in patients bearing HER2-overexpressing tumors as compared to others subtypes. Using quantitative PCR and immunoblotting, we showed that breast cancer cells with HER2-amplification (SKBR-3) have greater expression of PGC-1β as compared to a non-tumorous breast cell (MCF-10A) and higher proliferation rate. PGC-1β expression was knocked down with short interfering RNA in HER2-overexpressing cells, and cells decreased proliferation. In these PGC-1β-inhibited cells, we found increased citrate synthase activity and no marked changes in mitochondrial respiration. Glycolytic pathway was decreased, characterized by lower intracellular lactate levels. In addition, after PGC-1β knockdown, SKBR-3 cells showed increased reactive oxygen species production, no changes in antioxidant activity, and decreased expression of ERRα, a modulator of metabolism. In conclusion, we show an association of HER2-overexpression and PGC-1β. PGC-1β knockdown impairs HER2-overexpressing cells proliferation acting on ERRα signaling, metabolism, and redox balance. • Keywords: Breast cancer subtypes, HER2-overexpressing, PGC-1β, Proliferation, Human breast adenocarcinoma SKBR-3 cells
Labels: MiParea: Respiration, Genetic knockout;overexpression, Patients
Pathology: Cancer
Organism: Human Tissue;cell: Genital, Other cell lines Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET
Pathway: ROX
HRR: Oxygraph-2k
2016-01