Abstract
Capicua (CIC) is a highly conserved transcriptional repressor that is differentially regulated through mitogen-activated protein kinase (MAPK) signaling or genetic alteration across human cancer. CIC contributes to tumor progression and metastasis through direct transcriptional control of effector target genes. Recent findings indicate that CIC dysregulation is mechanistically linked and restricted to specific cancer subtypes, yet convergence on key downstream transcriptional nodes are critical for CIC-regulated oncogenesis across these cancers. In this review, we focus on how differential regulation of CIC through functional and genetic mechanisms contributes to subtype-specific cancer phenotypes and we propose new therapeutic strategies to effectively target CIC-altered cancers.
Copyright © 2020 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Antineoplastic Combined Chemotherapy Protocols / pharmacology
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Carcinogenesis / drug effects
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Carcinogenesis / genetics*
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Cell Proliferation / drug effects
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Cell Proliferation / genetics
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Drug Resistance, Neoplasm / drug effects
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Drug Resistance, Neoplasm / genetics
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Gene Expression Regulation, Neoplastic / drug effects
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Gene Expression Regulation, Neoplastic / genetics*
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Humans
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MAP Kinase Signaling System / drug effects
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MAP Kinase Signaling System / genetics
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Molecular Targeted Therapy / methods
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Neoplasms / drug therapy
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Neoplasms / genetics*
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Protein Processing, Post-Translational / drug effects
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Repressor Proteins / antagonists & inhibitors
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Repressor Proteins / genetics
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Repressor Proteins / metabolism*
Substances
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CIC protein, human
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Repressor Proteins