Spatholobus suberectusColumn Extract Inhibits Estrogen Receptor Positive Breast Cancer via Suppressing ER MAPK PI3K/AKT Pathway

Author:

Sun Jia-Qi1,Zhang Gan-Lin1,Zhang Yi1,Nan Nan1,Sun Xu1,Yu Ming-Wei1,Wang Hong2,Li Jin-Ping13ORCID,Wang Xiao-Min1ORCID

Affiliation:

1. Department of Oncology, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing, China

2. Beijing Institute of Traditional Chinese Medicine, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing, China

3. Department of Medical Biochemistry and Microbiology, Uppsala University, 75123 Uppsala, Sweden

Abstract

Although Chinese herbal compounds have long been alternatively applied for cancer treatment in China, their treatment effects have not been sufficiently investigated. The Chinese herbSpatholobus suberectusis commonly prescribed to cancer patients. HPLC analysis has shown that the main components ofSpatholobus suberectusare flavonoids that can be classified as phytoestrogens, having a structure similar to estrogen. This study was designed to investigate the effects ofSpatholobus suberectuscolumn extract (SSCE) on the estrogen receptor-positive (ER+) breast cancer cell line MCF-7 and its possible molecular mechanism. In our study, MTT assay was performed to evaluate cell viability. The results show that SSCE (80, 160, and 320 μg/ml) significantly decreased the viability of MCF-7 cells. SSCE also triggered apoptosis, arrested the cell cycle at the G0/G1 phase, and inhibited cell migration. A dual-luciferase reporter system showed that SSCE suppressed intranuclear p-ER activity; Western blot analysis confirmed the repressed expression of phosphorylated-ER alpha (p-ERα), ERK1/2, p-ERK1/2, AKT, p-AKT, p-mTOR, PI3K, and p-PI3K, indicating that SSCE suppressed the MAPK PI3K/AKT signaling pathway. Collectively, our results suggest that SSCE causes apoptosis, an arrest in the G0/G1 phase, and a decrease in migration in ER+ MCF-7 cells via hypoactivity of the ER and suppression of the MAPK PI3K/AKT pathway.

Funder

Beijing Municipal Natural Science Foundation

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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