Abstract
Triple negative breast cancers (TNBC) are clinically heterogeneous but mostly aggressive malignancies devoid of expression of the estrogen, progesterone and HER2 (ERBB2 or NEU) receptors. Recent evidence shows that basal endoplasmic reticulum stress (ERS) is typically activated in TNBC and cooperates with hypoxia signaling to promote tumor progression and relapse; ERS and hypoxia response may therefore be among the long-searched hallmarks of TNBC.
MeSH terms
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Basic Helix-Loop-Helix Transcription Factors / antagonists & inhibitors
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Basic Helix-Loop-Helix Transcription Factors / metabolism
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DNA-Binding Proteins / antagonists & inhibitors
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DNA-Binding Proteins / metabolism
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Endoplasmic Reticulum Stress
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Female
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Humans
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Hypoxia
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
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Neoplastic Stem Cells / metabolism
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Receptor, ErbB-2 / metabolism
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Receptors, Estrogen / metabolism
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Receptors, Progesterone / metabolism
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Recurrence
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Regulatory Factor X Transcription Factors
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Transcription Factors / antagonists & inhibitors
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Transcription Factors / metabolism
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Triple Negative Breast Neoplasms / metabolism*
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Triple Negative Breast Neoplasms / pathology
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Unfolded Protein Response
Substances
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BHLHE41 protein, human
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Basic Helix-Loop-Helix Transcription Factors
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DNA-Binding Proteins
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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Receptors, Estrogen
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Receptors, Progesterone
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Regulatory Factor X Transcription Factors
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Transcription Factors
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Receptor, ErbB-2