MITF controls the TCA cycle to modulate the melanoma hypoxia response

In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia‐associated transcription factor (MITF). The response to hypoxia is driven by hypoxia‐inducible transcription factors (HIFs) that repr...

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Vydané v:Pigment Cell & Melanoma Research Ročník 32; číslo 6; s. 792 - 808
Hlavní autori: Louphrasitthiphol, Pakavarin, Ledaki, Ioanna, Chauhan, Jagat, Falletta, Paola, Siddaway, Robert, Buffa, Francesca M., Mole, David R., Soga, Tomoyoshi, Goding, Colin R.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Wiley 01.11.2019
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John Wiley and Sons Inc
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ISSN:1755-1471, 1755-148X, 1755-148X
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Abstract In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia‐associated transcription factor (MITF). The response to hypoxia is driven by hypoxia‐inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA‐binding specificity, it is unclear whether they co‐regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up‐regulated by HIF1α and co‐regulates a subset of HIF targets including VEGFA. Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo‐hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.
AbstractList In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia‐associated transcription factor (MITF). The response to hypoxia is driven by hypoxia‐inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA‐binding specificity, it is unclear whether they co‐regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up‐regulated by HIF1α and co‐regulates a subset of HIF targets including VEGFA. Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo‐hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.
In response to the dynamic intra-tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia-associated transcription factor (MITF). The response to hypoxia is driven by hypoxia-inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA-binding specificity, it is unclear whether they co-regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up-regulated by HIF1α and co-regulates a subset of HIF targets including VEGFA. Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo-hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.In response to the dynamic intra-tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia-associated transcription factor (MITF). The response to hypoxia is driven by hypoxia-inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA-binding specificity, it is unclear whether they co-regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up-regulated by HIF1α and co-regulates a subset of HIF targets including VEGFA. Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo-hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.
In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia‐associated transcription factor (MITF). The response to hypoxia is driven by hypoxia‐inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA‐binding specificity, it is unclear whether they co‐regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up‐regulated by HIF1α and co‐regulates a subset of HIF targets including VEGFA. Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo‐hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.
In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the microphthalmia‐associated transcription factor (MITF). The response to hypoxia is driven by hypoxia‐inducible transcription factors (HIFs) that reprogram metabolism and promote angiogenesis. HIF1α indirectly represses MITF that can activate HIF1α expression. Although HIF and MITF share a highly related DNA‐binding specificity, it is unclear whether they co‐regulate subset of target genes. Moreover, the genomewide impact of hypoxia on melanoma and whether melanoma cell lines representing different phenotypic states exhibit distinct hypoxic responses is unknown. Here we show that three different melanoma cell lines exhibit widely different hypoxia responses with only a core 23 genes regulated in common after 12 hr in hypoxia. Surprisingly, under hypoxia MITF is transiently up‐regulated by HIF1α and co‐regulates a subset of HIF targets including VEGFA . Significantly, we also show that MITF represses itself and also regulates SDHB to control the TCA cycle and suppress pseudo‐hypoxia. Our results reveal a previously unsuspected role for MITF in metabolism and the network of factors underpinning the hypoxic response in melanoma.
Author Paola Falletta
Francesca M. Buffa
Robert Siddaway
Colin R. Goding
Ioanna Ledaki
Jagat Chauhan
Pakavarin Louphrasitthiphol
David R. Mole
Tomoyoshi Soga
AuthorAffiliation 1 Ludwig Institute for Cancer Research, Nuffield Department of Clinical Medicine University of Oxford Oxford UK
4 Institute for Advanced Biosciences Keio University Yamagata Japan
2 Department of Oncology University of Oxford Oxford UK
3 Target Discovery Institute, Nuffield Department of Clinical Medicine University of Oxford Oxford UK
AuthorAffiliation_xml – name: 4 Institute for Advanced Biosciences Keio University Yamagata Japan
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  surname: Goding
  fullname: Goding, Colin R.
  email: colin.goding@ludwig.ox.ac.uk
  organization: University of Oxford
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Issue 6
Keywords hypoxia
melanoma
genomewide
glucose limitation
MITF
Language English
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PublicationTitle Pigment Cell & Melanoma Research
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PublicationYear 2019
Publisher Wiley
Wiley Subscription Services, Inc
John Wiley and Sons Inc
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Snippet In response to the dynamic intra‐tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the...
In response to the dynamic intra-tumor microenvironment, melanoma cells adopt distinct phenotypic states associated with differential expression of the...
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StartPage 792
SubjectTerms Angiogenesis
Biotechnology
Cell Line, Tumor
Citric Acid Cycle
Deoxyribonucleic acid
DNA
Gene expression
Gene Expression Regulation, Neoplastic
Genes
Genome, Human
genomewide
glucose limitation
Humans
Hypoxia
Hypoxia-Inducible Factor 1, alpha Subunit
Hypoxia-Inducible Factor 1, alpha Subunit - metabolism
Melanoma
Melanoma - genetics
Melanoma - pathology
Metabolism
Microphthalmia-Associated Transcription Factor
Microphthalmia-Associated Transcription Factor - metabolism
MITF
Neoplasm Invasiveness
Original
Original Articles
Succinate Dehydrogenase
Succinate Dehydrogenase - metabolism
Transcription factors
transcription factors, TCA cycle, hypoxia, genomewide, glucose limitation, hypoxia, melanoma, MITF
Tricarboxylic acid cycle
Tumor Hypoxia
Tumor Hypoxia - genetics
Up-Regulation
Up-Regulation - genetics
Title MITF controls the TCA cycle to modulate the melanoma hypoxia response
URI https://cir.nii.ac.jp/crid/1870020692916763264
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fpcmr.12802
https://www.ncbi.nlm.nih.gov/pubmed/31207090
https://www.proquest.com/docview/2300557597
https://www.proquest.com/docview/2242816985
https://pubmed.ncbi.nlm.nih.gov/PMC6777998
Volume 32
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