AbstractBreast cancer, an epithelial cell-based cancer, has a very high incidence and mortality rate worldwide. Approximately 80% or more of breast cancers show evidence of elevated function of the hormone receptor estrogen receptor (ER), and hormone receptor-targeted endocrine therapy is applied during the course of treatment. However, approximately 30% of patients with ER-positive breast cancer are refractory to endocrine therapy, and the development of novel therapies and drugs for ER-positive breast cancer is expected. 慶應義塾大学先端生命科学研究所・特任准教授Institute for Advanced Biosciences, Keio University齊藤 康弘Yasuhiro Saito― 192 ―We have previously analyzed the pathophysiological roles of the cell polarity proteins LLGL2 and SCRIB in breast cancer and found that LLGL2 and SCRIB are important for the growth of ER-positive breast cancer cells. LLGL2 interacts with the amino acid transporter SLC7A5 and promotes the plasma membrane localization of SLC7A5, resulting in the uptake of the amino acid leucine from the extracellular to the intracellular space and enhancing cell proliferation of ER-positive breast cancer cells. Interestingly, leucine-dependent cell proliferation is specifically observed in ER-positive breast cancer cells, suggesting that enhanced SLC7A5 function is important for inducing drug resistance to the endocrine therapeutic drug tamoxifen. However, the molecular mechanisms underlying the leucine-dependent cell proliferation observed in ER-positive breast cancer cells and the acquisition of drug resistance by overexpression of SLC7A5 remain unclear, although the importance of leucine uptake into cells via SLC7A5 was demonstrated in the proliferation and drug resistance of ER-positive breast cancer cells However, the molecular mechanisms underlying the leucine-dependent cell proliferation observed in ER-positive breast cancer cells and the acquisition of drug resistance by overexpression of SLC7A5 remain unclear. In this study, we analyzed the molecular mechanism 乳がん細胞のロイシン依存的細胞増殖におけるグルタミンの機能解析Functional analysis of glutamine in leucine-dependent cell proliferation in breast cancer cells
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