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乳腺癌中的同类相食、细胞存活和内分泌抵抗。

Cannibalism, cell survival, and endocrine resistance in breast cancer.

机构信息

Department of Oncology, W405A Research Building, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA.

出版信息

Breast Cancer Res. 2011 Aug 12;13(4):311. doi: 10.1186/bcr2870.

Abstract

Breast cancer cells often respond to an endocrine therapy by altering expression of specific estrogen-responsive genes and inducing autophagy, a cannibalistic lysosomal pathway. Autophagy eliminates damaged or other organelles, allowing the recovery of the energy stored in their macromolecules to attempt restoration of metabolic homeostasis. Induction of autophagy can result from activation of the unfolded protein response following metabolic stress, the final cell fate often being determined by the extent and duration of autophagy. A study by Gonzalez-Malerva and colleagues builds upon this extensive knowledge, adding HSPB8 to the list of altered genes associated with endocrine resistance in breast cancer and describing the ability of HSPB8 to regulate autophagy and confer tamoxifen resistance.

摘要

乳腺癌细胞常通过改变特定雌激素反应基因的表达并诱导自噬(一种溶酶体途径的“自食”行为)来对内分泌治疗产生反应。自噬可消除受损或其他细胞器,从而恢复大分子物质中储存的能量,以尝试恢复代谢平衡。自噬的诱导可源于代谢应激后未折叠蛋白反应的激活,而最终的细胞命运通常由自噬的程度和持续时间决定。冈萨雷斯-马勒瓦(Gonzalez-Malerva)及其同事的研究在此基础上进一步拓展,将 HSPB8 添加到与乳腺癌内分泌耐药相关的改变基因列表中,并描述了 HSPB8 调节自噬和赋予他莫昔芬耐药的能力。

相似文献

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Autophagy and endocrine resistance in breast cancer.自噬与乳腺癌内分泌耐药。
Expert Rev Anticancer Ther. 2011 Aug;11(8):1283-94. doi: 10.1586/era.11.111.

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