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A TFAP2C Gene Signature is Predictive of Outcome in HER2-positive Breast Cancer
Journal article   Peer reviewed

A TFAP2C Gene Signature is Predictive of Outcome in HER2-positive Breast Cancer

Vincent T Wu, Boris Kiriazov, Kelsey E Koch, Vivian W Gu, Anna C Beck, Nicholas Borcherding, Tiandao Li, Peter Addo, Zachary J Wehrspan, Weizhou Zhang, …
Molecular cancer research, Vol.18(1), pp.46-56
01/2020
DOI: 10.1158/1541-7786.MCR-19-0359
PMID: 31619506

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Abstract

The AP-2γ transcription factor, encoded by the TFAP2C gene, regulates the expression of estrogen receptor-alpha (ERα) and other genes associated with hormone response in luminal breast cancer. Little is known about the role of AP-2γ in other breast cancer subtypes. A subset of HER2+ breast cancers with amplification of the TFAP2C gene locus becomes addicted to AP-2γ. Herein we sought to define AP-2γ gene targets in HER2+ breast cancer and identify genes accounting for physiologic effects of growth and invasiveness regulated by AP-2γ. Comparing HER2+ cell lines that demonstrated differential response to growth and invasiveness with knockdown of TFAP2C , we identified a set of 68 differentially expressed target genes. CDH5 and CDKN1A were among the genes differentially regulated by AP-2γ and that contributed to growth and invasiveness. Pathway analysis implicated the MAPK13 /p38δ and retinoic acid regulatory nodes, which were confirmed to display divergent responses in different HER2+ cancer lines. To confirm the clinical relevance of the genes identified, the AP-2γ gene signature was found to be highly predictive of outcome in HER2+ breast cancer patients. We conclude that AP-2γ regulates a set of genes in HER2+ breast cancer that drive cancer growth and invasiveness. The AP-2γ gene signature predicts outcome of patients with HER2+ breast cancer and pathway analysis predicts that subsets of patients will respond to drugs that target the MAPK or retinoic acid pathways.
Breast Cancer Transcription AP-2γ CDH5 CDKN1A HER2-positive MAPK13 Retinoic Acid TFAP2C

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