Abstract
O(2) deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coexist during tumor growth. The ability of cells to grow during hypoxia results in part from crosstalk between hypoxia-inducible factors (HIFs) and the proto-oncogene c-Myc. Acting alone, HIF and c-Myc partially regulate complex adaptations undertaken by tumor cells growing in low O(2). However, acting in concert these transcription factors reprogram metabolism, protein synthesis, and cell cycle progression, to "fine tune" adaptive responses to hypoxic environments.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Cell Hypoxia*
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Cell Proliferation*
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Gene Expression Regulation, Neoplastic
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / genetics
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism*
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Neoplasms / metabolism*
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Neoplasms / pathology
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Proto-Oncogene Mas
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism*
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Transcription, Genetic
Substances
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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MAS1 protein, human
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Proto-Oncogene Mas
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Proto-Oncogene Proteins c-myc