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PI3K/Akt信号通路在乳腺癌内分泌治疗耐药中的作用及对策 被引量:4

The Role and Application of the PI3K/Akt Signaling Pathway in Breast Cancer with Endocrine Therapy Resistance
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摘要 乳腺癌是女性最常见的肿瘤,大约75%的乳腺癌表达雌激素受体和/或孕激素受体。激素受体阳性的转移性乳腺癌患者通常采用内分泌治疗,然而由于内分泌治疗耐药的产生,其应用受到了限制。近年来发现,PI3K/Akt(丝氨酸/苏氨酸激酶)信号通路在乳腺癌的发展中发挥着重要作用。本文对PI3K/Akt信号通路在乳腺癌内分泌治疗耐药中的作用进行了综述,以期为雌激素受体阳性乳腺癌治疗提供新对策。 Breast cancer is the most common cancer among women, about 75% of breast cancers express the estrogen receptor and/or the progesterone receptor. Patients with hormone receptor-positive metastatic breast cancer are usually treated with endocrine therapy. However, due to the generation of endocrine therapy resistance, its application has been limited. Recently discovered, PI3K/Akt signaling pathway plays an important role in the development of breast cancer. In this paper, we specifically analyze the role of the PI3K/Akt signaling pathway in breast cancer endocrine therapy resistance, in order to offer new strategies to estrogen receptor-positive breast cancer.
作者 林阳 章斌
出处 《标记免疫分析与临床》 CAS 2015年第12期1287-1292,共6页 Labeled Immunoassays and Clinical Medicine
基金 苏州市科技发展计划项目 项目编号:SYS201458
关键词 乳腺癌 PI3K/AKT信号通路 内分泌治疗耐药 PI3K/Akt通路抑制剂 联合治疗 Breast cancer PI3K/Akt signaling pathway Endocrine therapy resistance Inhibition of thePI3K/Akt pathway Combination therapy
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  • 1Gao X, Zhang Y, Arrazola P, et al. Tsc tumour suppressor proteins antagonize amino-acid-TOR signalling. Nat Cell Biol 2002; 4:699-704.
  • 2Potter C J, Pedraza LG, Xu T. Akt regulates growth by directly phosphorylating Tsc2. Nat Cell Biol 2002; 4:658-665.
  • 3Goncharova EA, Goncharov DA, Eszterhas A, et al. Tuberin regulates p70 S6 kinase activation and ribosomal protein S6 phosphorylation. A role for the TSC2 tumor suppressor gene in pulmonary lymphangioleiomyomatosis (LAM). J Biol Chem 2002; 277:30958-30967.
  • 4Inoki K, Li Y, Zhu T, Wu J, Guan KL. TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling. Nat Cell Biol 2002; 4:648-657.
  • 5Potter C J, Huang H, Xu T. Drosophila Tsc I functions with Tsc2 to antagonize insulin signaling in regulating cell growth, cell proliferation, and organ size. Cell 2001; 105:357-368.
  • 6Tapon N, Ito N, Dickson B J, Treisman JE, Hariharan IK. The Drosophila tuberous sclerosis complex gene homologs restrict cell growth and cell proliferation. Cell 2001; 105:345-355.
  • 7Gao X, Pan D. TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth. Genes Dev 2001; 15:1383-1392.
  • 8Radimerski T, Montagne J, Hemmings-Mieszczak M, Thomas G. Lethality of Drosophila lacking TSC tumor suppressor function rescued by reducing dS6K signaling. Genes Dev 2002; 16:2627-2632.
  • 9Tee AR, Fingar DC, Manning BD, Kwiatkowski DJ, Cantley LC, Blenis J. Tuberous sclerosis complex- 1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling. Proc Natl Acad Sci USA 2002; 99:13571-13576.
  • 10Sabatini DM, Erdjument-Bromage H, Lui M, Tempst P, Snyder SH. RAFT 1: a mammalian protein that binds to FKBP 12 in a rapamycin-dependent fashion and is homologous to yeast TORs. Cell 1994; 78:35-43.

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