Induction of Caspase-dependent Apoptosis by Apigenin by Inhibiting STAT3 Signaling in HER2-overexpressing MDA-MB-453 Breast Cancer Cells
- Authors
- Seo, Hye-Sook; Ku, Jin Mo; Choi, Han-Seok; Woo, Jong-Kyu; Jang, Bo-Hyoung; Shin, Yong Cheol; Ko, Seong-Gyu
- Issue Date
- Jun-2014
- Publisher
- INT INST ANTICANCER RESEARCH
- Keywords
- Breast cancer; HER2; apigenin; apotosis; STAT3; VEGF
- Citation
- ANTICANCER RESEARCH, v.34, no.6, pp.2869 - 2882
- Journal Title
- ANTICANCER RESEARCH
- Volume
- 34
- Number
- 6
- Start Page
- 2869
- End Page
- 2882
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12591
- ISSN
- 0250-7005
- Abstract
- Background: This study aimed to examine the effect of apigenin on proliferation and apoptosis in HER2-overexpressing MDA-MB-453 breast cancer cells. Materials and Methods: The antiproliferative effects of apigenin were examined by proliferation and MTT assays. The effect of apigenin on apoptotic molecules was determined by western blotting. RT-PCR was performed to measure mRNA levels of HIF-1 alpha and VEGF. ELISA assay was performed to measure intracellular VEGF levels. Immunocytochemistry was performed to evaluate nuclear STAT3 level. Results: Apigenin inhibited the proliferation of MDA-MB-453 cells. Apigenin up-regulated the levels of cleaved caspase-8 and caspase-3, and induced the cleavage of PARP. Apigenin induced extrinsic apoptosis and blocked the activation (phosphorylation) of JAK2 and STAT3. Apigenin inhibited CoCl2-induced VEGF secretion and decreased the nuclear staining of STAT3. Conclusion: Apigenin exerts its antiproliferative activity by inhibiting STAT3 signaling. Apigenin could serve as a useful compound to prevent or treat HER2-overexpressing breast cancer.
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