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1
Expression of the telomerase catalytic subunit, hTERT, induces resistance to transforming growth factor beta growth inhibition in p16INK4A(-) human mammary epithelial cells.端粒酶催化亚基hTERT的表达可诱导p16INK4A（-）人乳腺上皮细胞对转化生长因子β生长抑制产生抗性。
Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4498-503. doi: 10.1073/pnas.071483998. Epub 2001 Apr 3.
2
Molecular changes accompanying senescence and immortalization of cultured human mammary epithelial cells.培养的人乳腺上皮细胞衰老和永生化过程中的分子变化。
Int J Biochem Cell Biol. 2002 Nov;34(11):1382-94. doi: 10.1016/s1357-2725(02)00047-x.
3
Events in the immortalizing process of primary human mammary epithelial cells by the catalytic subunit of human telomerase.人端粒酶催化亚基使原代人乳腺上皮细胞永生化过程中的事件。
Biochem J. 2002 Aug 1;365(Pt 3):765-72. doi: 10.1042/BJ20011848.
4
Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics.表达hTERT并绕过限制寿命的p16(INK4a)强制机制的人类角质形成细胞会变得永生化，但仍保留正常的生长和分化特征。
Mol Cell Biol. 2000 Feb;20(4):1436-47. doi: 10.1128/MCB.20.4.1436-1447.2000.
5
Raf-1-induced growth arrest in human mammary epithelial cells is p16-independent and is overcome in immortal cells during conversion.Raf-1诱导的人乳腺上皮细胞生长停滞不依赖p16，且在永生化细胞转化过程中被克服。
Oncogene. 2002 Sep 12;21(41):6328-39. doi: 10.1038/sj.onc.1205780.
6
Gradual phenotypic conversion associated with immortalization of cultured human mammary epithelial cells.与培养的人乳腺上皮细胞永生化相关的渐进性表型转化。
Mol Biol Cell. 1997 Dec;8(12):2391-405. doi: 10.1091/mbc.8.12.2391.
7
Genetic and epigenetic changes in human epithelial cells immortalized by telomerase.端粒酶永生化的人上皮细胞中的遗传和表观遗传变化。
Am J Pathol. 2000 May;156(5):1537-47. doi: 10.1016/S0002-9440(10)65025-0.
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A novel human cancer culture model for the study of prostate cancer.一种用于前列腺癌研究的新型人类癌症培养模型。
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Comparison of human mammary epithelial cells immortalized by simian virus 40 T-Antigen or by the telomerase catalytic subunit.由猿猴病毒40大T抗原或端粒酶催化亚基永生化的人乳腺上皮细胞的比较
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Telomerase activation by c-Myc in human mammary epithelial cells requires additional genomic changes.c-Myc在人乳腺上皮细胞中激活端粒酶需要其他基因组改变。
Cell Cycle. 2009 Oct 15;8(20):3373-8. doi: 10.4161/cc.8.20.9856. Epub 2009 Oct 19.

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Telomerase in Cancer: Function, Regulation, and Clinical Translation.癌症中的端粒酶：功能、调控及临床转化
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Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.超越细胞衰老的细胞老化：体外和体内细胞周期停滞前的衰老标志物。
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The non-canonical functions of telomerase: to turn off or not to turn off.端粒酶的非经典功能：关闭还是不关闭。
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Different culture media modulate growth, heterogeneity, and senescence in human mammary epithelial cell cultures.不同的培养基可调节人乳腺上皮细胞培养物的生长、异质性和衰老。
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Transforming growth factor-β in liver cancer stem cells and regeneration.肝癌干细胞与再生中的转化生长因子-β
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GWAS of epigenetic aging rates in blood reveals a critical role for TERT.血液表观遗传衰老速度的全基因组关联研究揭示了 TERT 的关键作用。
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8
Friend or foe? Telomerase as a pharmacological target in cancer and cardiovascular disease.敌友难辨？端粒酶作为癌症和心血管疾病的药物靶点
Pharmacol Res. 2016 Sep;111:422-433. doi: 10.1016/j.phrs.2016.07.003. Epub 2016 Jul 6.
9
TGF-β/β2-spectrin/CTCF-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.转化生长因子-β/β2-血影蛋白/CCCTC结合因子调控人类干细胞疾病贝克威思-维德曼综合征中的肿瘤抑制作用。
J Clin Invest. 2016 Feb;126(2):527-42. doi: 10.1172/JCI80937. Epub 2016 Jan 19.
10
A TORC2-Akt Feed-Forward Topology Underlies HER3 Resiliency in HER2-Amplified Cancers.TORC2-Akt前馈拓扑结构是HER2扩增型癌症中HER3弹性的基础。
Mol Cancer Ther. 2015 Dec;14(12):2805-17. doi: 10.1158/1535-7163.MCT-15-0403. Epub 2015 Oct 5.

本文引用的文献

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Culture models of human mammary epithelial cell transformation.人乳腺上皮细胞转化的培养模型
J Mammary Gland Biol Neoplasia. 2000 Oct;5(4):365-78. doi: 10.1023/a:1009525827514.
2
The ZNF217 gene amplified in breast cancers promotes immortalization of human mammary epithelial cells.
Cancer Res. 2001 Feb 15;61(4):1250-4.
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The role of senescence and immortalization in carcinogenesis.衰老与永生化在致癌过程中的作用。
Carcinogenesis. 2000 Mar;21(3):477-84. doi: 10.1093/carcin/21.3.477.
4
Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics.表达hTERT并绕过限制寿命的p16(INK4a)强制机制的人类角质形成细胞会变得永生化，但仍保留正常的生长和分化特征。
Mol Cell Biol. 2000 Feb;20(4):1436-47. doi: 10.1128/MCB.20.4.1436-1447.2000.
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p57KIP2 expression and loss of heterozygosity during immortal conversion of cultured human mammary epithelial cells.培养的人乳腺上皮细胞永生化转化过程中的p57KIP2表达及杂合性缺失
Cancer Res. 1999 Oct 15;59(20):5112-8.
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Creation of human tumour cells with defined genetic elements.利用特定遗传元件创建人类肿瘤细胞。
Nature. 1999 Jul 29;400(6743):464-8. doi: 10.1038/22780.
7
Viral oncogenes accelerate conversion to immortality of cultured conditionally immortal human mammary epithelial cells.病毒癌基因可加速培养的条件性永生化人乳腺上皮细胞向永生化状态的转变。
Oncogene. 1999 Apr 1;18(13):2169-80. doi: 10.1038/sj.onc.1202523.
8
Expression of catalytically active telomerase does not prevent premature senescence caused by overexpression of oncogenic Ha-Ras in normal human fibroblasts.在正常人成纤维细胞中，具有催化活性的端粒酶的表达并不能阻止由致癌性Ha-Ras过表达所导致的早衰。
Cancer Res. 1999 Apr 1;59(7):1539-43.
9
Absence of cancer-associated changes in human fibroblasts immortalized with telomerase.用端粒酶永生化的人成纤维细胞中不存在癌症相关变化。
Nat Genet. 1999 Jan;21(1):115-8. doi: 10.1038/5063.
10
Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype.人类体细胞中的端粒酶表达不会诱导与转化表型相关的变化。
Nat Genet. 1999 Jan;21(1):111-4. doi: 10.1038/5056.

端粒酶催化亚基hTERT的表达可诱导p16INK4A（-）人乳腺上皮细胞对转化生长因子β生长抑制产生抗性。

Expression of the telomerase catalytic subunit, hTERT, induces resistance to transforming growth factor beta growth inhibition in p16INK4A(-) human mammary epithelial cells.

作者信息

Stampfer M R, Garbe J, Levine G, Lichtsteiner S, Vasserot A P, Yaswen P

机构信息

Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA 94720, USA.

出版信息

Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4498-503. doi: 10.1073/pnas.071483998. Epub 2001 Apr 3.

DOI:10.1073/pnas.071483998
PMID:11287649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC31863/
Abstract

Failures to arrest growth in response to senescence or transforming growth factor beta (TGF-beta) are key derangements associated with carcinoma progression. We report that activation of telomerase activity may overcome both inhibitory pathways. Ectopic expression of the human telomerase catalytic subunit, hTERT, in cultured human mammary epithelial cells (HMEC) lacking both telomerase activity and p16(INK4A) resulted in gaining the ability to maintain indefinite growth in the absence and presence of TGF-beta. The ability to maintain growth in TGF-beta was independent of telomere length and required catalytically active telomerase capable of telomere maintenance in vivo. The capacity of ectopic hTERT to induce TGF-beta resistance may explain our previously described gain of TGF-beta resistance after reactivation of endogenous telomerase activity in rare carcinogen-treated HMEC. In those HMEC that overcame senescence, both telomerase activity and TGF-beta resistance were acquired gradually during a process we have termed conversion. This effect of hTERT may model a key change occurring during in vivo human breast carcinogenesis.

摘要

无法对衰老或转化生长因子β（TGF-β）作出生长停滞反应是与癌症进展相关的关键紊乱现象。我们报告称，端粒酶活性的激活可能会克服这两种抑制途径。在缺乏端粒酶活性和p16（INK4A）的培养人乳腺上皮细胞（HMEC）中，人端粒酶催化亚基hTERT的异位表达导致细胞在有无TGF-β的情况下都获得了维持无限生长的能力。在TGF-β存在的情况下维持生长的能力与端粒长度无关，并且需要能够在体内维持端粒的具有催化活性的端粒酶。异位hTERT诱导TGF-β抗性的能力可能解释了我们之前所描述的，在经致癌物处理的罕见HMEC中内源性端粒酶活性重新激活后出现的TGF-β抗性增加现象。在那些克服了衰老的HMEC中，端粒酶活性和TGF-β抗性都是在一个我们称为转化的过程中逐渐获得的。hTERT的这种作用可能模拟了人类乳腺肿瘤发生过程中发生的一个关键变化。