Antiproliferative Effects of Soy Derived Dipeptides in Human Breast Cancer Cell Lines

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 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. Hinute‐AM was solubilized in 0.1% FA and analyzed by LC‐MS/MS. The data analysis has revealed the presence of five peptides (VPY, EL, IQ, LQ and YG) in Hinute‐AM. Out of these, three synthetic peptides (YG, LQ and IQ) were tested for their effects on proliferation of three normal (12A, 12F and 184A1) and four breast cancer cells (HCC1806, MCF 7, BT‐549 and MDA‐MB‐231). All peptides had significant antiproliferative effects in all breast cancer cell lines. However, the major effect was with YG and in particular in HCC1806 cell line. We reported earlier that expression of TSPO (translocator protein) is higher in breast cancer cells than normal breast cells. PCNA is also regarded as good cell proliferation marker. In this experiment, we studied the effects of YG on TSPO and PCNA expression in normal and three breast cancer cells (MCF‐ 7, BT‐549 and HCC‐1806 by immunohistochemistry. Results indicated that YG down‐regulated the expression of both TSPO and PCNA in all cancer cells. Furthermore, the binding capacity of 3 H Ro5‐4864 to the TSPO receptors was significantly reduced by both YG and LQ. The mechanism by which YG and LQ inhibited the proliferation of breast cancer cell lines is under investigation. (Supported by grants from Fuji Oil Company, Osaka, Japan and NIH 5U54MD007593) Support or Funding Information Supported by grants from Fuji Oil Company, Osaka, Japan and NIH 5U54MD007593 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .