A Feedback Loop Comprising EGF/TGFα Sustains TFCP2-Mediated Breast Cancer Progression
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- Yi Zhao
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
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- Neha Kaushik
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
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- Jae-Hyeok Kang
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
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- Nagendra Kumar Kaushik
- 2Plasma Bioscience Research Center, Applied Plasma Medicine Center, Department of Electrical and Biological Physics, Kwangwoon University, Seoul, South Korea.
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- Seung Han Son
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
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- Nizam Uddin
- 3Center for Cell Analysis & Modeling, University of Connecticut Health Center, Farmington, Connecticut.
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- Min-Jung Kim
- 4Laboratory of Radiation Exposure and Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, South Korea.
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- Chul Geun Kim
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
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- Su-Jae Lee
- 1Department of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea.
説明
<jats:title>Abstract</jats:title> <jats:sec> <jats:title /> <jats:p>Stemness and epithelial–mesenchymal transition (EMT) are two fundamental characteristics of metastasis that are controlled by diverse regulatory factors, including transcription factors. Compared with other subtypes of breast cancer, basal-type or triple-negative breast cancer (TNBC) has high frequencies of tumor relapse. However, the role of alpha-globin transcription factor CP2 (TFCP2) has not been reported as an oncogenic driver in those breast cancers. Here, we show that TFCP2 is a potent factor essential for EMT, stemness, and metastasis in breast cancer. TFCP2 directly bound promoters of EGF and TGFα to regulate their expression and stimulate autocrine signaling via EGFR. These findings indicate that TFCP2 is a new antimetastatic target and reveal a novel regulatory mechanism in which a positive feedback loop comprising EGF/TGFα and AKT can control malignant breast cancer progression.</jats:p> </jats:sec> <jats:sec> <jats:title>Significance:</jats:title> <jats:p>TFCP2 is a new antimetastatic target that controls TNBC progression via a positive feedback loop between EGF/TGFα and the AKT signaling axis.</jats:p> </jats:sec>
収録刊行物
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- Cancer Research
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Cancer Research 80 (11), 2217-2229, 2020-06-01
American Association for Cancer Research (AACR)