Inhibition of monocarboxyate transporter 1 by AZD3965 as a novel therapeutic approach for diffuse large B-cell lymphoma and Burkitt lymphoma
Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy...
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| Published in | Haematologica (Roma) Vol. 102; no. 7; pp. 1247 - 1257 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Italy
Ferrata Storti Foundation
01.07.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0390-6078 1592-8721 1592-8721 |
| DOI | 10.3324/haematol.2016.163030 |
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| Abstract | Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients' tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed
: daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks
resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death
and reduced CA46 disease burden
These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors. |
|---|---|
| AbstractList | Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients’ tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed in vivo: daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks in vitro resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death in vitro and reduced CA46 disease burden in vivo. These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors. Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients' tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed in vivo: daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks in vitro resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death in vitro and reduced CA46 disease burden in vivo These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors.Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients' tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed in vivo: daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks in vitro resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death in vitro and reduced CA46 disease burden in vivo These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors. Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients’ tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed in vivo : daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks in vitro resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death in vitro and reduced CA46 disease burden in vivo . These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors. Inhibition of monocarboxylate transporter 1 has been proposed as a therapeutic approach to perturb lactate shuttling in tumor cells that lack monocarboxylate transporter 4. We examined the monocarboxylate transporter 1 inhibitor AZD3965, currently in phase I clinical studies, as a potential therapy for diffuse large B-cell lymphoma and Burkitt lymphoma. Whilst extensive monocarboxylate transporter 1 protein was found in 120 diffuse large B-cell lymphoma and 10 Burkitt lymphoma patients' tumors, monocarboxylate transporter 4 protein expression was undetectable in 73% of the diffuse large B-cell lymphoma samples and undetectable or negligible in each Burkitt lymphoma sample. AZD3965 treatment led to a rapid accumulation of intracellular lactate in a panel of lymphoma cell lines with low monocarboxylate transporter 4 protein expression and potently inhibited their proliferation. Metabolic changes induced by AZD3965 in lymphoma cells were consistent with a feedback inhibition of glycolysis. A profound cytostatic response was also observed : daily oral AZD3965 treatment for 24 days inhibited CA46 Burkitt lymphoma growth by 99%. Continuous exposure of CA46 cells to AZD3965 for 7 weeks resulted in a greater dependency upon oxidative phosphorylation. Combining AZD3965 with an inhibitor of mitochondrial complex I (central to oxidative phosphorylation) induced significant lymphoma cell death and reduced CA46 disease burden These data support clinical examination of AZD3965 in Burkitt lymphoma and diffuse large B-cell lymphoma patients with low tumor monocarboxylate transporter 4 expression and highlight the potential of combination strategies to optimally target the metabolic phenotype of tumors. |
| Author | Crossland, Rachel Blair, Helen Long, Anna Critchlow, Susan E. Miwa, Satomi Noble, Richard A. Bell, Natalie Keun, Hector C. Phillips, Nicole Nakjang, Sirintra Thomas, Huw Rand, Vikki Sikka, Arti Televantou, Despina Wedge, Stephen R. Bacon, Chris M. Bomken, Simon |
| AuthorAffiliation | 5 MRC/EPSRC Newcastle Molecular Pathology Node, Newcastle upon Tyne 2 Division of Cancer, Imperial College London 6 Department of Pediatric and Adolescent Hematology and Oncology, Newcastle upon Tyne Hospitals NHS Foundation Trust 4 Cellular Pathology, Newcastle upon Tyne Hospitals NHS Foundation Trust 7 AstraZeneca, Cambridge, UK 1 Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne 3 Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne |
| AuthorAffiliation_xml | – name: 2 Division of Cancer, Imperial College London – name: 3 Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne – name: 6 Department of Pediatric and Adolescent Hematology and Oncology, Newcastle upon Tyne Hospitals NHS Foundation Trust – name: 4 Cellular Pathology, Newcastle upon Tyne Hospitals NHS Foundation Trust – name: 5 MRC/EPSRC Newcastle Molecular Pathology Node, Newcastle upon Tyne – name: 1 Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne – name: 7 AstraZeneca, Cambridge, UK |
| Author_xml | – sequence: 1 givenname: Richard A. surname: Noble fullname: Noble, Richard A. – sequence: 2 givenname: Natalie surname: Bell fullname: Bell, Natalie – sequence: 3 givenname: Helen surname: Blair fullname: Blair, Helen – sequence: 4 givenname: Arti surname: Sikka fullname: Sikka, Arti – sequence: 5 givenname: Huw surname: Thomas fullname: Thomas, Huw – sequence: 6 givenname: Nicole surname: Phillips fullname: Phillips, Nicole – sequence: 7 givenname: Sirintra surname: Nakjang fullname: Nakjang, Sirintra – sequence: 8 givenname: Satomi surname: Miwa fullname: Miwa, Satomi – sequence: 9 givenname: Rachel surname: Crossland fullname: Crossland, Rachel – sequence: 10 givenname: Vikki surname: Rand fullname: Rand, Vikki – sequence: 11 givenname: Despina surname: Televantou fullname: Televantou, Despina – sequence: 12 givenname: Anna surname: Long fullname: Long, Anna – sequence: 13 givenname: Hector C. surname: Keun fullname: Keun, Hector C. – sequence: 14 givenname: Chris M. surname: Bacon fullname: Bacon, Chris M. – sequence: 15 givenname: Simon surname: Bomken fullname: Bomken, Simon – sequence: 16 givenname: Susan E. surname: Critchlow fullname: Critchlow, Susan E. – sequence: 17 givenname: Stephen R. surname: Wedge fullname: Wedge, Stephen R. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28385782$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Biomarkers Burkitt Lymphoma - drug therapy Burkitt Lymphoma - genetics Burkitt Lymphoma - metabolism Burkitt Lymphoma - pathology Cell Death - drug effects Cell Line, Tumor Drug Resistance, Neoplasm Electron Transport Complex I - antagonists & inhibitors Energy Metabolism - drug effects Humans Lactic Acid - metabolism Lymphoma, Large B-Cell, Diffuse - drug therapy Lymphoma, Large B-Cell, Diffuse - genetics Lymphoma, Large B-Cell, Diffuse - metabolism Lymphoma, Large B-Cell, Diffuse - pathology Mitochondria - drug effects Mitochondria - metabolism Monocarboxylic Acid Transporters - antagonists & inhibitors Monocarboxylic Acid Transporters - genetics Monocarboxylic Acid Transporters - metabolism Muscle Proteins - genetics Muscle Proteins - metabolism Oxidative Phosphorylation - drug effects Pyrimidinones - pharmacology Pyrimidinones - therapeutic use Symporters - antagonists & inhibitors Symporters - genetics Symporters - metabolism Thiophenes - pharmacology Thiophenes - therapeutic use |
| Title | Inhibition of monocarboxyate transporter 1 by AZD3965 as a novel therapeutic approach for diffuse large B-cell lymphoma and Burkitt lymphoma |
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