Introduction: Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor (ER), progesterone receptor (PgR), and epidermal growth factor receptor 2 (HER2), currently has no effective hormonal or molecular target therapy. Objective and Methods: To elucidate the role of the mammalian target of rapamycin (mTOR) signaling pathway in TNBC, the expression of molecules involved in mTOR signaling including mTOR, phosphorylated (p)-mTOR, p-4EBP1, GLUT1, GLUT3, HIF-1α, and Ki67 was investigated by immunohistochemistry in 35 TNBC and 81 non-TNBC cases. Results: Expression of p-mTOR, the activated form of mTOR, but not unphosphorylated mTOR, was significantly higher in non-TNBC cases than in TNBC cases. Expression of p-4EBP1, GLUT1, and GLUT3 was higher in TNBC cases than in non-TNBC cases. When the localization of p-mTOR was classified as nuclear, perinuclear, or cytoplasmic, nuclear localization of p-mTOR was observed more frequently in TNBC than in non-TNBC cases and was correlated with the expression of GLUT1 and GLUT3, which was related to proliferation activity examined with Ki67. Conclusions: mTOR signaling regulates cell proliferation in some cases of TNBC and may be a potential target of molecular therapy for TNBC.

中文翻译：

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mTOR信号通路分子在三阴性乳腺癌中的表达

简介：三阴性乳腺癌（TNBC）缺乏雌激素受体（ER）、孕激素受体（PgR）和表皮生长因子受体2（HER2）的表达，目前没有有效的激素或分子靶向治疗。目的和方法：阐明哺乳动物雷帕霉素靶蛋白 (mTOR) 信号通路在 TNBC 中的作用，参与 mTOR 信号传导的分子包括 mTOR、磷酸化 (p)-mTOR、p-4EBP1、GLUT1、GLUT3、HIF- 1α 和 Ki67 在 35 例 TNBC 和 81 例非 TNBC 病例中通过免疫组织化学进行了研究。结果：非 TNBC 病例中 p-mTOR（mTOR 的活化形式，而非未磷酸化的 mTOR）的表达显着高于 TNBC 病例。TNBC 病例中 p-4EBP1、GLUT1 和 GLUT3 的表达高于非 TNBC 病例。当 p-mTOR 的定位被归类为核、核周或细胞质时，在 TNBC 中比在非 TNBC 病例中更频繁地观察到 p-mTOR 的核定位，并且与 GLUT1 和 GLUT3 的表达相关，后者与Ki67 检测增殖活性。结论：mTOR 信号在某些 TNBC 病例中调节细胞增殖，可能是 TNBC 分子治疗的潜在靶点。