Apigenin induces apoptosis by suppressing Bcl-xl and Mcl-1 simultaneously via signal transducer and activator of transcription 3 signaling in colon cancer
| Autor: | Shuji Takiguchi, Masayasu Hara, Kenta Saito, Hideyuki Ishiguro, Yoichi Matsuo, Hiroki Takahashi, Yuzo Maeda, Tomotaka Okubo, Takahisa Hirokawa, Nozomu Nakai, Takeshi Yanagita, Kazuyoshi Shiga, Nanako Ando |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cancer Research Small interfering RNA Oncogene biology Bcl-xL 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine Oncology chemistry Apoptosis 030220 oncology & carcinogenesis Apigenin Cancer cell STAT protein biology.protein Cancer research STAT3 |
| Zdroj: | International journal of oncology. 52(5) |
| ISSN: | 1791-2423 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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