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Induction of p-glycoprotein, glutathione-s-transferase-pi, catalase, C-fos and C-erbb1 in rodent cell-lines after exposure to Doxorubicin, ethanol and caffeine.在啮齿动物细胞系中,暴露于阿霉素、乙醇和咖啡因后p-糖蛋白、谷胱甘肽-S-转移酶-pi、过氧化氢酶、C-fos和C-erbb1的诱导情况。
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Happyhour, a Ste20 family kinase, implicates EGFR signaling in ethanol-induced behaviors.“快乐时光”蛋白,一种Ste20家族激酶,在乙醇诱导的行为中涉及表皮生长因子受体信号传导。
Cell. 2009 May 29;137(5):949-60. doi: 10.1016/j.cell.2009.03.020. Epub 2009 May 21.
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Resistance to endocrine therapy: are breast cancer stem cells the culprits?内分泌治疗耐药:乳腺癌干细胞是罪魁祸首吗?
J Mammary Gland Biol Neoplasia. 2009 Mar;14(1):45-54. doi: 10.1007/s10911-009-9115-y. Epub 2009 Feb 28.
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Anti-epidermal growth factor receptor monoclonal antibody cetuximab inhibits EGFR/HER-2 heterodimerization and activation.抗表皮生长因子受体单克隆抗体西妥昔单抗可抑制表皮生长因子受体/人表皮生长因子受体2异源二聚化及激活。
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Cancer stem cells: how can we target them?癌症干细胞:我们如何靶向作用于它们?
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Cadherins and cancer: how does cadherin dysfunction promote tumor progression?钙黏蛋白与癌症:钙黏蛋白功能障碍如何促进肿瘤进展?
Oncogene. 2008 Nov 24;27(55):6920-9. doi: 10.1038/onc.2008.343.
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Her2-positive breast cancer: herceptin and beyond.人表皮生长因子受体2阳性乳腺癌:赫赛汀及其他治疗方法
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Understanding and treating triple-negative breast cancer.了解和治疗三阴性乳腺癌。
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EGFR 可能将适量饮酒与乳腺癌风险增加联系起来。

EGFR may couple moderate alcohol consumption to increased breast cancer risk.

机构信息

Purdue University School of Pharmacy, Purdue University Center for Cancer Research, West Lafayette, IN, USA.

Purdue University Department of Psychological Sciences, West Lafayette, IN, USA.

出版信息

Breast Cancer (Dove Med Press). 2009 Oct 5;1:31-8. doi: 10.2147/bctt.s6254.

DOI:10.2147/bctt.s6254
PMID:24367161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2872252/
Abstract

Alcohol consumption is an established risk factor for breast cancer. Nonetheless, the mechanism by which alcohol contributes to breast tumor initiation or progression has yet to be definitively established. Studies using cultured human tumor cell lines have identified signaling molecules that may contribute to the effects of alcohol, including reactive oxygen species and other ethanol metabolites, matrix metalloproteases, the ErbB2/Her2/Neu receptor tyrosine kinase, cytoplasmic protein kinases, adenylate cyclase, E-cadherins, estrogen receptor, and a variety of transcription factors. Emerging data suggest that the epidermal growth factor receptor (EGFR) tyrosine kinase may contribute to breast cancer genesis and progression. Here we integrate these findings and propose three mechanisms by which alcohol contributes to breast cancer. A common feature of these mechanisms is increased EGFR signaling. Finally, we discuss how these mechanisms suggest strategies for addressing the risks associated with alcohol consumption.

摘要

饮酒是乳腺癌的既定风险因素。尽管如此,酒精促进乳腺肿瘤发生或进展的机制尚未得到明确证实。使用培养的人肿瘤细胞系进行的研究已经确定了可能有助于酒精作用的信号分子,包括活性氧和其他乙醇代谢物、基质金属蛋白酶、ErbB2/Her2/Neu 受体酪氨酸激酶、细胞质蛋白激酶、腺苷酸环化酶、E-钙黏蛋白、雌激素受体和多种转录因子。新出现的数据表明,表皮生长因子受体(EGFR)酪氨酸激酶可能有助于乳腺癌的发生和发展。在这里,我们整合了这些发现,并提出了酒精促进乳腺癌发生的三种机制。这些机制的一个共同特征是 EGFR 信号的增加。最后,我们讨论了这些机制如何为解决与饮酒相关的风险提供策略。