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Breast Cancer Res. 2004;6(4):162-3. doi: 10.1186/bcr904. Epub 2004 Jun 9.
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Activation of extracellular signal-regulated kinase and c-Jun-NH(2)-terminal kinase but not p38 mitogen-activated protein kinases is required for RRR-alpha-tocopheryl succinate-induced apoptosis of human breast cancer cells.RRR-α-生育酚琥珀酸酯诱导人乳腺癌细胞凋亡需要细胞外信号调节激酶和c-Jun氨基末端激酶的激活，而p38丝裂原活化蛋白激酶则不需要。
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MAP kinase/estrogen receptor cross-talk enhances estrogen-mediated signaling and tumor growth but does not confer tamoxifen resistance.丝裂原活化蛋白激酶/雌激素受体相互作用增强雌激素介导的信号传导和肿瘤生长，但不赋予他莫昔芬耐药性。
Oncogene. 2002 Jun 6;21(25):4000-8. doi: 10.1038/sj.onc.1205506.
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Estrogens do not modify MAP kinase-dependent nuclear signaling during stimulation of early G(1) progression in human breast cancer cells.在刺激人乳腺癌细胞早期G(1)期进程期间，雌激素不会改变丝裂原活化蛋白激酶依赖性核信号传导。
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Pyk2 and FAK regulate neurite outgrowth induced by growth factors and integrins.Pyk2和粘着斑激酶（FAK）调节生长因子和整合素诱导的神经突生长。
Nat Cell Biol. 2000 Sep;2(9):574-81. doi: 10.1038/35023515.
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Hypoxic activation of nuclear factor-kappa B is mediated by a Ras and Raf signaling pathway and does not involve MAP kinase (ERK1 or ERK2).核因子-κB的缺氧激活由Ras和Raf信号通路介导，且不涉及丝裂原活化蛋白激酶（ERK1或ERK2）。
Cancer Res. 1994 Oct 15;54(20):5273-9.
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Activation of mitogen-activated protein kinase in estrogen receptor alpha-positive breast cancer cells in vitro induces an in vivo molecular phenotype of estrogen receptor alpha-negative human breast tumors.体外雌激素受体α阳性乳腺癌细胞中丝裂原活化蛋白激酶的激活可诱导雌激素受体α阴性人类乳腺肿瘤的体内分子表型。
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Novel signaling molecules implicated in tumor-associated fatty acid synthase-dependent breast cancer cell proliferation and survival: Role of exogenous dietary fatty acids, p53-p21WAF1/CIP1, ERK1/2 MAPK, p27KIP1, BRCA1, and NF-kappaB.与肿瘤相关脂肪酸合酶依赖性乳腺癌细胞增殖和存活相关的新型信号分子：外源性膳食脂肪酸、p53-p21WAF1/CIP1、ERK1/2 MAPK、p27KIP1、BRCA1和NF-κB的作用
Int J Oncol. 2004 Mar;24(3):591-608.
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Prevention of cytokine-induced apoptosis by insulin-like growth factor-I is independent of cell adhesion molecules in HT29-D4 colon carcinoma cells-evidence for a NF-kappaB-dependent survival mechanism.胰岛素样生长因子-I对细胞因子诱导的凋亡的预防作用在HT29-D4结肠癌细胞中独立于细胞粘附分子——一种NF-κB依赖的存活机制的证据
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Growth factor signalling in endocrine and anti-growth factor resistant breast cancer.内分泌及抗生长因子耐药性乳腺癌中的生长因子信号传导
Rev Endocr Metab Disord. 2007 Sep;8(3):241-53. doi: 10.1007/s11154-007-9033-5.

本文引用的文献

1
A cytoplasmic substrate of mitogen-activated protein kinase is responsible for estrogen receptor-alpha down-regulation in breast cancer cells: the role of nuclear factor-kappaB.丝裂原活化蛋白激酶的一种细胞质底物负责乳腺癌细胞中雌激素受体α的下调：核因子κB的作用。
Mol Endocrinol. 2004 Jun;18(6):1396-410. doi: 10.1210/me.2004-0048. Epub 2004 Mar 31.
2
Tumour necrosis factor and PI3-kinase control oestrogen receptor alpha protein level and its transrepression function.
Br J Cancer. 2004 Feb 23;90(4):853-9. doi: 10.1038/sj.bjc.6601541.
3
Nonendocrine pathways and endocrine resistance: observations with antiestrogens and signal transduction inhibitors in combination.非内分泌途径与内分泌抵抗：抗雌激素与信号转导抑制剂联合应用的观察结果
Clin Cancer Res. 2004 Jan 1;10(1 Pt 2):346S-54S. doi: 10.1158/1078-0432.ccr-031206.
4
Specific inhibition of DNMT1 by antisense oligonucleotides induces re-expression of estrogen receptor-alpha (ER) in ER-negative human breast cancer cell lines.反义寡核苷酸对DNA甲基转移酶1（DNMT1）的特异性抑制可诱导雌激素受体α（ER）在ER阴性的人乳腺癌细胞系中重新表达。
Cancer Biol Ther. 2003 Sep-Oct;2(5):552-6. doi: 10.4161/cbt.2.5.469.
5
Multiple mechanisms of estrogen receptor gene repression contribute to ER-negative breast cancer.
Pharmacogenomics J. 2003;3(5):251-3. doi: 10.1038/sj.tpj.6500201.
6
Heregulin-beta1 regulates the estrogen receptor-alpha gene expression and activity via the ErbB2/PI 3-K/Akt pathway.Heregulin-β1通过ErbB2/PI 3-K/Akt信号通路调控雌激素受体α基因的表达及活性。
Oncogene. 2003 Apr 10;22(14):2073-87. doi: 10.1038/sj.onc.1206311.
7
Farnesyltransferase inhibitor (L-744,832) restores TGF-beta type II receptor expression and enhances radiation sensitivity in K-ras mutant pancreatic cancer cell line MIA PaCa-2.法尼基转移酶抑制剂（L-744,832）可恢复转化生长因子-β II型受体表达，并增强K-ras突变型胰腺癌细胞系MIA PaCa-2的辐射敏感性。
Oncogene. 2002 Nov 7;21(51):7883-90. doi: 10.1038/sj.onc.1205948.
8
Hyperactivation of MAPK induces loss of ERalpha expression in breast cancer cells.丝裂原活化蛋白激酶（MAPK）的过度激活会导致乳腺癌细胞中雌激素受体α（ERα）表达缺失。
Mol Endocrinol. 2001 Aug;15(8):1344-59. doi: 10.1210/mend.15.8.0678.
9
Constitutive activation of NF-kappaB during progression of breast cancer to hormone-independent growth.在乳腺癌进展为激素非依赖性生长过程中NF-κB的组成性激活。
Mol Cell Biol. 1997 Jul;17(7):3629-39. doi: 10.1128/MCB.17.7.3629.

Extreme growth factor signalling can promote oestrogen receptor-alpha loss: therapeutic implications in breast cancer.

作者信息

Gee Julia M W, Giles Martin G, Nicholson Robert I

机构信息

Tenovus Centre for Cancer Research, Welsh School of Pharmacy, Cardiff University, CF10 3XF, Wales, UK.

出版信息

Breast Cancer Res. 2004;6(4):162-3. doi: 10.1186/bcr904. Epub 2004 Jun 9.

DOI:10.1186/bcr904
PMID:15217488
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC468673/
Abstract
摘要