Abstract
Allicin induces apoptosis in various carcinoma cells and inhibits tumorigenesis. Activating transcription factor 3 (ATF3) is a stress‐inducible gene and known as a transcription factor to induce or inhibit target genes. However, the precise mechanism of allicin‐induced apoptosis is still unclear in human breast cancer cells. We investigated the effect of allicin on cell proliferation, apoptosis, and its pathway in MCF‐7 cells. MTT assay and western blotting showed that allicin decreased concentration‐dependently cell proliferation, induced apoptosis related proteins (Bax, Bid, AIF) and activated caspase‐3 and 8 in a concentration dependent manner, respectively. Our data also showed that allicin increased phosphorylation of ERK1/2, p38 and JNK in a concentration‐and time‐dependent manner and protein level of ATF3. In addition, MTT assay and western blotting showed that allicin treatment resulted in decreased cell proliferation and high level expression of apoptosis related proteins in ATF3‐overexpressed MCF‐7 cells, respectively, suggesting that ATF3 expression is involved in the regulation of allicin‐induced apoptosis. Taken together, the data suggest that allicin induces apoptosis through MAPKs and ATF3 signaling pathways in MCF‐7 cells.
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