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Antiproliferative Effects of Hinute‐AM in Human Breast Cancer Cell Lines
Author(s) -
Mukherjee Shyamali,
Mitra Piyali,
Ratna Anuradha,
Maebuchi Motohiro,
Furuta Hitoshi,
Das Salil K
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.842.3
Subject(s) - breast cancer , soy protein , cancer , cancer research , cell growth , hydrolysate , medicine , dmba , cancer cell , endocrinology , chemistry , biochemistry , carcinogenesis , hydrolysis
Breast cancer is a debilitating disease that affects women worldwide. In the United States, breast cancer is the second leading cause of cancer‐related deaths in women. Diet is an important factor in the development of numerous diseases, including breast cancer. We reported earlier that the consumption of soy protein controlled not only the proliferation of dimethylbenz [a] anthracene (DMBA)‐induced breast cancer cells in rats but also its aggressiveness. Soy protein is hydrolyzed in the gut to small peptides which are easily absorbed and are involved in various cellular functions. Fuji Oil Company, Osaka, Japan, has commercially marketed a soy protein hydrolysate, termed Hinute‐AM, composed of primarily di‐ and tripeptides, to be used as a health food. This product was found to have anti‐inflammatory property. It is possible that the antiproliferative effects of soy protein on breast cancer in rats may be mediated by its hydrolysis in the small intestine to small peptides. Hence, we hypothesized that the beneficial effect of soy protein in breast cancer development may be mediated by its hydrolysis product as peptides. Several normal (MCF 10A, 12A, and 184 A1), triple negative (MDA–MB‐231, BT‐549 and HCC‐1806) and steroid receptor positive (T47D and MCH 7) breast cancer cell lines were treated with different concentrations of Hinute‐AM for 24 h. Hinute‐AM at both low and high concentrations did not have any significant effect on proliferation of normal cells. However, while it inhibited proliferation of all breast cancer cell lines at low concentration (0.02–0.10 mg/ml), at high concentration (0.5–2.0 mg/ml), it had no effect. Furthermore, while Hinute‐AM had no effect on the levels of Ki‐67 and cyclin D1 levels in normal cells, it significantly decreased their levels in all breast cancer cell lines. The mechanism by which Hinute‐AM inhibits proliferation of breast cancer cell lines is under investigation. Support or Funding Information (Supported by grants from Fuji Oil Company, Osaka, Japan and NIH 5U54MD007593)