Sulkowska Mariola, Golaszewska Jolanta, Wincewicz Andrzej, Koda Mariusz, Baltaziak Marek, Sulkowski Stanislaw
Department of Pathology, Collegium Pathologicum, Medical University of Bialystok, Bialystok, 15-269, Poland.
Pathol Oncol Res. 2006;12(2):69-72. doi: 10.1007/BF02893446. Epub 2006 Jun 24.
Leptin restricts intake of calories as a satiety hormone. It probably stimulates neoplastic proliferation in breast cancer, too. Growth of malignant cells could be regulated by various leptin-induced second messengers like STAT3 (signal transducers and activators of transcription 3), AP-1 (transcription activator protein 1), MAPK (mitogen-activated protein kinase) and ERKs (extracellular signal-regulated kinases). They seem to be involved in aromatase expression, generation of estrogens and activation of estrogen receptor alpha (ERalpha) in malignant breast epithelium. Leptin may maintain resistance to antiestrogen therapy. Namely, it increased activation of estrogen receptors, therefore, it was suspected to reduce or even overcome the inhibitory effect of tamoxifen on breast cell proliferation. Although several valuable reviews have been focused on the role of leptin in breast cancer, the status of knowledge in this field changes quickly and our insight should be continuously revised. In this summary, we provide refreshed interpretation of intensively reported scientific queries of the topic.
瘦素作为一种饱腹感激素，可限制热量摄入。它可能也会刺激乳腺癌中的肿瘤细胞增殖。恶性细胞的生长可能受多种瘦素诱导的第二信使调节，如信号转导和转录激活因子3（STAT3）、转录激活蛋白1（AP-1）、丝裂原活化蛋白激酶（MAPK）和细胞外信号调节激酶（ERK）。它们似乎参与了恶性乳腺上皮中芳香化酶的表达、雌激素的生成以及雌激素受体α（ERα）的激活。瘦素可能维持对抗雌激素治疗的耐药性。也就是说，它增强了雌激素受体的激活，因此，人们怀疑它会降低甚至克服他莫昔芬对乳腺细胞增殖的抑制作用。尽管已有几篇有价值的综述聚焦于瘦素在乳腺癌中的作用，但该领域的知识状况变化迅速，我们的见解应不断更新。在本综述中，我们对该主题中大量报道的科学问题提供了新的解读。
