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Peptides in common bean ( Phaseolus vulgaris L.) non‐digestible fraction inhibit human colorectal cancer cell survival in vitro through oxidative stress injury: a comparative study (644.5)
Author(s) -
LunaVital Diego,
De Mejia Elvira,
Dia Vermont,
LoarcaPina Guadalupe
Publication year - 2014
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.28.1_supplement.644.5
Subject(s) - phaseolus , oxidative stress , apoptosis , survivin , antioxidant , cell cycle , cell cycle checkpoint , colorectal cancer , reactive oxygen species , biochemistry , chemistry , microbiology and biotechnology , biology , cancer , botany , genetics
The aim was to characterize peptides present in non‐digestible fraction (NDF) of common bean cultivars, Azufrado Higuera (AH) and Bayo Madero (BM), produced after pepsin‐pancreatin digestion, determine their antiproliferative action on human colorectal cancer cells and their mechanism of action. Five peptides represented 70% of total protein in both cultivars (GLTSK, LSGNK, GEGSGA, MPACGSS and MTEEY). HCT116 colorectal cancer cell line was most sensitive to bean AH (IC 50 =0.53 mg/mL), and RKO to BM (IC 50 =0.51 mg/mL) peptide extracts. Cultivars AH and BM increased significantly the expression of p53 in HCT116 cells by 76% and 68%, respectively. AH modified the expression of cell cycle regulation proteins p21 (64%) and cyclin B1 (‐45%). BM modified the expression of apoptosis‐related proteins BAD (22%); cytC (66%), c‐casp3 (115%); Bax (50%), Bcl‐x (‐41%); Livin (‐32%); Survivin (‐27%) and TNFR1 (‐51%). Moreover, peptide extracts of both cultivars modified the expression of oxidative stress response‐related genes. In HCT116, NRF2‐related antioxidant enzymes were up‐regulated. Glutathione redox‐related enzymes were down‐regulated in RKO, potentially causing reactive oxygen species imbalance. In conclusion, peptides in common bean NDF contributed to the antiproliferative effect on human colorectal cancer cells by modifying molecules involved in cell cycle progression and apoptosis. Grant Funding Source : Supported by University of Illinois‐University of Queretaro research grants