The nutritional herb Epimedium grandiflorum inhibits the growth in a model for the Luminal A molecular subtype of breast cancer
Affiliations: Cancer Prevention Research Program, Palindrome Liaisons Consultants, Montvale, NJ 07645‑1559, USA, American Foundation for Chinese Medicine, Inc., Long Island, NY 11103‑0905, USA, Skin of Color Research Institute, Hampton University, Hampton, VA 23668, USA, Hackensack University Medical Center, Hackensack, NJ 07601, USA
- Published online on: February 13, 2017 https://doi.org/10.3892/ol.2017.5720
- Pages: 2477-2482
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The Luminal A subtype of breast cancer expresses the estrogen receptor (ER)-α and progesterone receptor (PR), but not the human epidermal growth factor receptor (HER)‑2 oncogene. This subtype of breast cancer responds to endocrine therapy involving the use of selective estrogen receptor modulators and/or inhibitors of estrogen biosynthesis. However, these therapeutic agents are frequently associated with long‑term systemic toxicity and acquired tumor resistance, emphasizing the need to identify non‑toxic alternative treatments for chemo‑endocrine therapy responsive breast cancer. The present study utilized the human mammary carcinoma‑derived, ER+/PR+/HER‑2‑ MCF‑7 cell line as a model of the Luminal A subtype of breast cancer to examine the growth inhibitory effect of the Chinese nutritional herb Epimedium grandiflorum (EG) and determine the mechanisms underlying this effect. MCF‑7 cells maintained in a serum‑depleted culture medium retained their ability to grow in response to 17β‑estradiol (E2). Treatment of the MCF‑7 cells with EG resulted in dose‑dependent inhibition of E2‑promoted growth. Mechanistically, EG inhibited E2‑promoted cell cycle progression through G1 stage arrest and modulated the cellular metabolism of E2, increasing the formation of the anti‑proliferative metabolites 2‑hydroxyestrone and estriol. Long‑term treatment of MCF‑7 cells with EG inhibited E2‑promoted anchorage independent growth, a surrogate in vitro biomarker of tumorigenesis. In conclusion, the results of the present study demonstrate the growth inhibitory effects of EG on MCF‑7 cells and identified clinically relevant mechanistic leads for its anti‑tumorigenic efficacy.