Abstract Title:

Apigenin induces apoptosis by suppressing Bcl-xl and Mcl-1 simultaneously via signal transducer and activator of transcription 3 signaling in colon cancer.

Abstract Source:

Int J Oncol. 2018 Mar 7. Epub 2018 Mar 7. PMID: 29512707

Abstract Author(s):

Yuzo Maeda, Hiroki Takahashi, Nozomu Nakai, Takeshi Yanagita, Nanako Ando, Tomotaka Okubo, Kenta Saito, Kazuyoshi Shiga, Takahisa Hirokawa, Masayasu Hara, Hideyuki Ishiguro, Yoichi Matsuo, Shuji Takiguchi

Article Affiliation:

Yuzo Maeda


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.

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