2. Academic Validation
  3. Genistin attenuates cellular growth and promotes apoptotic cell death breast cancer cells through modulation of ERalpha signaling pathway

Genistin attenuates cellular growth and promotes apoptotic cell death breast cancer cells through modulation of ERalpha signaling pathway

  • Life Sci. 2020 Dec 15;263:118594. doi: 10.1016/j.lfs.2020.118594.
Sun Tae Hwang 1,  Min Hee Yang 2,  Seung Ho Baek 3,  Jae-Young Um 1,  Kwang Seok Ahn 4
Affiliations

Affiliations

  • 1 Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea.
  • 2 Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea; KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Republic of Korea.
  • 3 College of Korean Medicine, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326, Republic of Korea.
  • 4 Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea; KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Republic of Korea. Electronic address: ksahn@khu.ac.kr.
PMID: 33075375 DOI: 10.1016/j.lfs.2020.118594
Abstract

Estrogen Receptor alpha (ERα) is a vital molecular target in ER-positive breast Cancer. Genistin (GS) is one of Isoflavones that can exert diverse pharmacological effects including that of anti-proliferation, anti-tumor angiogenesis, induce cell cycle arrest and Apoptosis. Here, we examined the efficacy of GS as an anti-cancer agent against breast Cancer cells. We observed that GS exhibited more cytotoxic activity against MCF-7 cells than MDA-MB-231cells. We found that GS caused negative regulation of ERα. It also effectively down-modulated ER nuclear translocation as well DNA binding activity in breast Cancer cells. Moreover, GS effectively induced Apoptosis and suppressed levels of oncogenic markers in MCF-7 cells. Interestingly, in ERα knocked-down MCF-7 cells, cell viability was found to be increased and the levels of cleaved PARP was abolished. We found completely contrasting results in ERα overexpressed MDA-MB-231 cells, where cell viability was decreased and expression level of apoptotic markers was enhanced. Our results demonstrate that GS can suppress ERα signaling and can be useful for prevention and therapy of ER-positive breast Cancer.

Keywords

Apoptosis; Breast cancer; Estrogen receptor alpha; Genistin.

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