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Cancers (Basel). 2018 Dec 27;11(1). pii: E23. doi: 10.3390/cancers11010023.

Effects of SAHA and EGCG on Growth Potentiation of Triple-Negative Breast Cancer Cells.

Author information

1
Department of Biology, University of Alabama at Birmingham, 1300 University Blvd, Birmingham, AL 35294, USA. klalewis@uab.edu.
2
School of Nursing, University of Alabama at Birmingham, 1701 University Blvd, Birmingham, AL 35294, USA. klalewis@uab.edu.
3
Department of Biology, University of Alabama at Birmingham, 1300 University Blvd, Birmingham, AL 35294, USA. hjordan@uab.edu.
4
Department of Biology, University of Alabama at Birmingham, 1300 University Blvd, Birmingham, AL 35294, USA. trygve@uab.edu.
5
Comprehensive Cancer Center, University of Alabama at Birmingham, 1802 6th Avenue South, Birmingham, AL 35294, USA. trygve@uab.edu.
6
Comprehensive Center for Healthy Aging, University of Alabama at Birmingham, 1530 3rd Avenue South, Birmingham, AL 35294, USA. trygve@uab.edu.
7
Nutrition Obesity Research Center, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294, USA. trygve@uab.edu.
8
Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, USA. trygve@uab.edu.

Abstract

Triple-negative breast cancer comprises approximately 15⁻20% of all breast cancers diagnosed and is nearly twice as common in black women than white women in the United States. We evaluated the effects of two epigenetic-modifying compounds on markers of growth potential in several triple-negative breast cancer cell lines. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor currently used in the treatment of cutaneous T cell lymphoma, was administered to triple-negative breast cancer cells alone or in combination with epigallocatechin-3-gallate (EGCG), a DNA methyltransferase (DNMT) inhibitor isolated from green tea. The compounds affected the expression of oncogenic miR-221/222 and tumor suppressors, p27 and PTEN, in addition to estrogen receptor alpha (ERα). E-cadherin expression was increased while N-cadherin was decreased, indicating a more epithelial phenotype. In addition, the activity of DNMTs was diminished with the treatments, and there was a significant enrichment of AcH3 within the promoter of p27 and PTEN, suggesting a role of epigenetic mechanisms for the aforementioned changes. These results translated to reduced migration of the triple-negative breast cancer cells with the treatments. Together, these findings support the role of SAHA and EGCG in limiting growth and proliferation of breast cancer cells.

KEYWORDS:

DNMT inhibitors; HDAC inhibitors; Mesenchymal-to-epithelial transition; breast cancer; cancer epigenetics; microRNA; phytochemicals

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