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Soy peptide lunasin induces PTEN‐mediated apoptosis in human breast cancer cells
Author(s) -
Pabona John Mark Pascua,
Dave Bhuvanesh,
Rahal Omar,
Lumen Ben O,
Mejia Elvira,
Simmen Rosalia CM
Publication year - 2011
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.25.1_supplement.213.3
Subject(s) - pten , cancer research , apoptosis , biology , genistein , protein kinase b , endocrinology , medicine , pi3k/akt/mtor pathway , biochemistry
The tumor suppressor PTEN inhibits the AKT signaling pathway whose unrestrained activity underlies many human malignancies. Previously we showed that dietary intake of soy protein isolate (SPI) enhanced PTEN expression in mammary tissue of rats with lower NMU‐induced mammary tumor incidence relative to those fed casein‐based diet. While epidemiological studies corroborate the breast cancer protective effects of soy, specifically of the major soy isoflavone genistein (GEN), the identity of other bioactive soy components remains relatively unknown. Here we evaluated the effects of lunasin, a soybean peptide previously detected in sera of rats and humans consuming soy‐rich diets, on PTEN‐mediated apoptosis of the mammary carcinoma cell line MCF‐7. Lunasin (2 μM >50 nM) increased PTEN expression and nuclear localization (by 2.5‐fold); enhanced PTEN‐mediated cellular apoptosis (by 10–15‐fold); and altered levels of p53 (increased) and p21 WAF1 (decreased) transcripts (P<0.05). GEN (2 μM >20 nM) elicited similar effects as lunasin on PTEN expression and PTEN‐mediated apoptosis in MCF‐7 cells. Lunasin and GEN are known to regulate core histone acetylation by which PTEN promoter activity is similarly controlled. Findings suggest that activation of PTEN expression by bioactive soy components, possibly via epigenetic mechanisms may underlie breast cancer protection. [USDA‐CRIS; Department of Defense BCRP]