Luteolin suppresses androgen receptor-positive triple-negative breast cancer cell proliferation and metastasis by epigenetic regulation of MMP9 expression via the AKT/mTOR signaling pathway

PI3K/AKT/mTOR通路 癌症研究 木犀草素 蛋白激酶B 雄激素受体 三阴性乳腺癌 雌激素受体 生物 乳腺癌 转移 细胞生长 信号转导 癌症 细胞生物学 前列腺癌 类黄酮 生物化学 遗传学 抗氧化剂
作者
Han‐Tsang Wu,Joseph Lin,Yi-En Liu,Hsiao‐Fan Chen,Kai‐Wen Hsu,Shu-Hsuan Lin,Kai‐Yen Peng,Kuo-Juei Lin,Chang‐Chi Hsieh,Dar‐Ren Chen
出处
期刊:Phytomedicine [Elsevier BV]
卷期号:81: 153437-153437 被引量:123
标识
DOI:10.1016/j.phymed.2020.153437
摘要

Triple-negative breast cancer (TNBC) represents up to 20% of all breast cancers. This cancer lacks the expression of the estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. The current therapeutic strategy for patients with this subtype is the use of cytotoxic chemotherapy and surgery. Luteolin is a natural herbal flavonoid and a potential therapeutic candidate for multiple diseases. The use of a treatment that combines Chinese herbal medicine and western medicine is rising in Asia. The present study evaluates the effects and molecular mechanisms involved with luteolin treatment and evaluates whether this herb affects androgen receptor-positive breast cancer cell proliferation or metastasis. In vitro evaluation of the effect of luteolin on androgen receptor-positive TNBC cell proliferation and metastasis Cell viability analysis was used for the cytotoxicity test. Colony formation and Bromodeoxyuridine (BrdU) staining-based proliferation experiments were used for cell proliferation. Wound healing and transwell assays were used for in vitro migration/invasion. The RT-qPCR analysis was used for gene expression. Furthermore, ChIP-qPCR analysis was used for epigenetic modification of gene promoters. Luteolin significantly inhibited the proliferation and metastasis of androgen receptor-positive TNBC. Furthermore, luteolin inactivated the AKT/mTOR signaling pathway and reversed the epithelial-mesenchymal transition (EMT). The combination of luteolin and inhibitors of AKT/mTOR synergistically repressed an androgen receptor-positive TNBC cell proliferation and metastasis. Luteolin also downregulated MMP9 expression by decreasing the levels of the AKT/mTOR promoting H3K27Ac and H3K56A on the MMP9 promoter region. Our findings indicate that luteolin inhibited the proliferation and metastasis of androgen receptor-positive TNBC by regulating MMP9 expression through a reduction in the levels of AKT/mTOR-inducing H3K27Ac and H3K56Ac.
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