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- Title
Apigenin induces apoptosis by suppressing Bcl-xl and Mcl-1 simultaneously via signal transducer and activator of transcription 3 signaling in colon cancer.
- Authors
Maeda, Yuzo; Takahashi, Hiroki; Nakai, Nozomu; Yanagita, Takeshi; Ando, Nanako; Okubo, Tomotaka; Saito, Kenta; Shiga, Kazuyoshi; Hirokawa, Takahisa; Hara, Masayasu; Ishiguro, Hideyuki; Matsuo, Yoichi; Takiguchi, Shuji
- Abstract
Apigenin is a natural flavonoid that exhibits anti-proliferative activity and induces apoptosis in various types of cancer, including colon cancer. The aim of the present study was to determine the mechanism underlying the apoptosis-inducing effect of apigenin in colon cancer. Apigenin reduced the proliferation of colon cancer cell lines, stimulated the cleavage of PARP and induced apoptosis in a dose-dependent manner. Apigenin treatment also suppressed the expression of the anti-apoptotic proteins Bcl-xL and Mcl-1. Small interfering RNA was used to knockdown Bcl-xL and Mcl-1 expression alone and in concert, and the proliferation and apoptosis of cancer cells were subsequently measured. The knockdown of Bcl-xL and Mcl-1 expression together markedly suppressed cell proliferation and induced apoptosis. Apigenin treatment also inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which targets Bcl-xL and Mcl-1. The results of the current study therefore determined that apigenin induces the apoptosis of colon cancer cells by inhibiting the phosphorylation of STAT3 and consequently downregulates the anti-apoptotic proteins Bcl-xL and Mcl-1.
- Publication
International Journal of Oncology, 2018, Vol 52, Issue 5, p1661
- ISSN
1019-6439
- Publication type
Article
- DOI
10.3892/ijo.2018.4308