Open AccessNisin, an apoptogenic bacteriocin and food preservative, attenuates HNSCC tumorigenesis via CHAC 1
Author(s) -
Joo Nam E.,
Ritchie Kathryn,
Kamarajan Pachiyappan,
Miao Di,
Kapila Yvonne L.
Publication year - 2012
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.35
Subject(s) - nisin , head and neck squamous cell carcinoma , apoptosis , carcinogenesis , chemistry , cancer research , cell growth , microbiology and biotechnology , biology , cancer , biochemistry , genetics , head and neck cancer , gene , antimicrobial , organic chemistry
Nisin, a bacteriocin and commonly used food preservative, may serve as a novel potential therapeutic for treating head and neck squamous cell carcinoma ( HNSCC ), as it induces preferential apoptosis, cell cycle arrest, and reduces cell proliferation in HNSCC cells, compared with primary keratinocytes. Nisin also reduces HNSCC tumorigenesis in vivo. Mechanistically, nisin exerts these effects on HNSCC , in part, through CHAC 1, a proapoptotic cation transport regulator, and through a concomitant CHAC 1‐independent influx of extracellular calcium. In addition, although CHAC 1 is known as an apoptotic mediator, its effects on cancer cell apoptosis have not been examined. Our studies are the first to report CHAC 1's new role in promoting cancer cell apoptosis under nisin treatment. These data support the concept that nisin decreases HNSCC tumorigenesis in vitro and in vivo by inducing increased cell apoptosis and decreased cell proliferation; effects that are mediated by activation of CHAC 1, increased calcium influxes, and induction of cell cycle arrest. These findings support the use of nisin as a potentially novel therapeutic for HNSCC , and as nisin is safe for human consumption and currently used in food preservation, its translation into a clinical setting may be facilitated.