Notch在甲状腺C细胞发育及甲状腺髓样癌治疗中的作用
Notch in the development of thyroid C-cells and the treatment of medullary thyroid cancer.
作者信息
Cook Mackenzie, Yu Xiao-Min, Chen Herbert
机构信息
Section of Endocrine Surgery, Department of Surgery, University of Wisconsin Madison, Wisconsin.
出版信息
Am J Transl Res. 2010 Feb 10;2(1):119-25.
Abstract
The Notch pathway plays an important role in the normal development of neuroendocrine cells, including the calcitonin producing C-cells of the thyroid. This effect has been elucidated to be mediated through modulation of Achaete-Scute Complex Like 1 (ASCL1), a transcription factor associated with poor prognosis in neuroendocrine cancer. Medullary thyroid cancer (MTC) is one of the neuroendocrine cancers derived from the thyroid C-cells. The Notch pathway has been shown to be inactive in MTC which may lead to altered expression of ASCL1. Artificial induction of Notch signaling in MTC cells can suppress ASCL1 expression, the cell growth as well as hormone secreting potential. Pharmacological activation of the Notch pathway also successfully suppresses the tumor growth in an animal model, which sheds light on the targeted therapy of Notch as a potential treatment for intractable MTC.
摘要
Notch信号通路在神经内分泌细胞的正常发育中起重要作用，包括甲状腺产生降钙素的C细胞。已阐明这种作用是通过调节类Achaete-Scute复合体1（ASCL1）介导的，ASCL1是一种与神经内分泌癌预后不良相关的转录因子。甲状腺髓样癌（MTC）是源自甲状腺C细胞的神经内分泌癌之一。已证明Notch信号通路在MTC中无活性，这可能导致ASCL1表达改变。在MTC细胞中人工诱导Notch信号可抑制ASCL1表达、细胞生长以及激素分泌潜能。Notch信号通路的药理学激活在动物模型中也成功抑制了肿瘤生长，这为将Notch作为难治性MTC的潜在治疗方法进行靶向治疗提供了思路。
相似文献
1
Notch in the development of thyroid C-cells and the treatment of medullary thyroid cancer.Notch在甲状腺C细胞发育及甲状腺髓样癌治疗中的作用
Am J Transl Res. 2010 Feb 10;2(1):119-25.
2
Overexpression of the NOTCH1 intracellular domain inhibits cell proliferation and alters the neuroendocrine phenotype of medullary thyroid cancer cells.NOTCH1细胞内结构域的过表达抑制细胞增殖并改变甲状腺髓样癌细胞的神经内分泌表型。
J Biol Chem. 2006 Dec 29;281(52):39819-30. doi: 10.1074/jbc.M603578200. Epub 2006 Nov 7.
3
Xanthohumol inhibits the neuroendocrine transcription factor achaete-scute complex-like 1, suppresses proliferation, and induces phosphorylated ERK1/2 in medullary thyroid cancer.黄腐酚抑制神经内分泌转录因子 Achaete-scute 复合物样 1，抑制增殖，并诱导甲状腺髓样癌细胞中磷酸化 ERK1/2。
Am J Surg. 2010 Mar;199(3):315-8; discussion 318. doi: 10.1016/j.amjsurg.2009.08.034.
4
Small cell lung cancer, an epithelial to mesenchymal transition (EMT)-like cancer: significance of inactive Notch signaling and expression of achaete-scute complex homologue 1.小细胞肺癌，一种类似上皮-间质转化（EMT）的癌症：无活性Notch信号传导的意义及achaete-scute复合体同源物1的表达
Hum Cell. 2017 Jan;30(1):1-10. doi: 10.1007/s13577-016-0149-3. Epub 2016 Oct 26.
5
Suberoyl bis-hydroxamic acid activates Notch-1 signaling and induces apoptosis in medullary thyroid carcinoma cells.辛二酰双羟肟酸激活Notch-1信号通路并诱导甲状腺髓样癌细胞凋亡。
Oncologist. 2008 Feb;13(2):98-104. doi: 10.1634/theoncologist.2007-0190.
6
Upregulation of ASCL1 and inhibition of Notch signaling pathway characterize progressive astrocytoma.ASCL1的上调和Notch信号通路的抑制是进展性星形细胞瘤的特征。
Oncogene. 2005 Oct 27;24(47):7073-83. doi: 10.1038/sj.onc.1208865.
7
Thiocoraline alters neuroendocrine phenotype and activates the Notch pathway in MTC-TT cell line.硫代珊瑚素改变神经内分泌表型并激活 MTC-TT 细胞系中的 Notch 通路。
Cancer Med. 2013 Oct;2(5):734-43. doi: 10.1002/cam4.118. Epub 2013 Sep 17.
8
The role of human achaete-scute homolog-1 in medullary thyroid cancer cells.人类毛状体-无刚毛同源物1在甲状腺髓样癌细胞中的作用。
Surgery. 2003 Dec;134(6):866-71; discussion 871-3. doi: 10.1016/s0039-6060(03)00418-5.
9
Differentiation of medullary thyroid cancer by C-Raf-1 silences expression of the neural transcription factor human achaete-scute homolog-1.通过C-Raf-1对甲状腺髓样癌进行分化可使神经转录因子人类无翅型MMTV整合位点家族成员1的表达沉默。
Surgery. 1996 Aug;120(2):168-72; discussion 173. doi: 10.1016/s0039-6060(96)80284-4.
10
Medullary thyroid cancer: the functions of raf-1 and human achaete-scute homologue-1.甲状腺髓样癌：raf-1和人类achaete-scute同源物-1的功能
Thyroid. 2005 Jun;15(6):511-21. doi: 10.1089/thy.2005.15.511.
引用本文的文献
1
Notch signaling pathway in cancer: from mechanistic insights to targeted therapies. Notch 信号通路与癌症：从机制研究到靶向治疗。
Signal Transduct Target Ther. 2024 May 27;9(1):128. doi: 10.1038/s41392-024-01828-x.
2
DLL3 (delta-like protein 3) expression correlates with stromal desmoplasia and lymph node metastases in medullary thyroid carcinomas.DLL3（δ样蛋白3）表达与甲状腺髓样癌的间质促纤维增生及淋巴结转移相关。
Endocr Connect. 2021 Mar;10(3):283-289. doi: 10.1530/EC-20-0611.
3
Notch Signaling in Thyroid Cancer. Notch 信号通路在甲状腺癌中的作用。
Adv Exp Med Biol. 2021;1287:155-168. doi: 10.1007/978-3-030-55031-8_10.
4
Notch3 as a novel therapeutic target in metastatic medullary thyroid cancer.Notch3作为转移性甲状腺髓样癌的新型治疗靶点。
Surgery. 2018 Jan;163(1):104-111. doi: 10.1016/j.surg.2017.07.039. Epub 2017 Nov 8.
5
Targeted Therapy for Medullary Thyroid Cancer: A Review.甲状腺髓样癌的靶向治疗：综述
Front Oncol. 2017 Oct 6;7:238. doi: 10.3389/fonc.2017.00238. eCollection 2017.
6
MiR-182 promotes cancer invasion by linking RET oncogene activated NF-κB to loss of the HES1/Notch1 regulatory circuit.微小RNA-182通过将RET致癌基因激活的核因子κB与HES1/Notch1调控回路的缺失相联系来促进癌症侵袭。
Mol Cancer. 2017 Jan 26;16(1):24. doi: 10.1186/s12943-016-0563-x.
7
Aberrant Activation of Notch Signaling Inhibits PROX1 Activity to Enhance the Malignant Behavior of Thyroid Cancer Cells.Notch信号通路的异常激活抑制PROX1活性以增强甲状腺癌细胞的恶性行为。
Cancer Res. 2016 Feb 1;76(3):582-93. doi: 10.1158/0008-5472.CAN-15-1199. Epub 2015 Nov 25.
8
Induction of apoptosis and autophagy in metastatic thyroid cancer cells by valproic acid (VPA).丙戊酸（VPA）诱导转移性甲状腺癌细胞凋亡和自噬
Int J Clin Exp Pathol. 2015 Jul 1;8(7):8291-7. eCollection 2015.
9
Identification of novel thyroid cancer-related genes and chemicals using shortest path algorithm.使用最短路径算法鉴定新型甲状腺癌相关基因和化学物质。
Biomed Res Int. 2015;2015:964795. doi: 10.1155/2015/964795. Epub 2015 Mar 22.
10
Tumor-suppressor role of Notch3 in medullary thyroid carcinoma revealed by genetic and pharmacological induction.遗传和药理学诱导揭示Notch3在甲状腺髓样癌中的肿瘤抑制作用
Mol Cancer Ther. 2015 Feb;14(2):499-512. doi: 10.1158/1535-7163.MCT-14-0073. Epub 2014 Dec 15.
本文引用的文献
1
Notch signaling: the core pathway and its posttranslational regulation.Notch信号通路：核心途径及其翻译后调控
Dev Cell. 2009 May;16(5):633-47. doi: 10.1016/j.devcel.2009.03.010.
2
Multi-targeted approach in the treatment of thyroid cancer.甲状腺癌的多靶点治疗方法。
Ther Clin Risk Manag. 2008 Oct;4(5):935-47. doi: 10.2147/tcrm.s3062.
3
Carcinoid tumors.类癌肿瘤
Oncologist. 2008 Dec;13(12):1255-69. doi: 10.1634/theoncologist.2008-0207. Epub 2008 Dec 17.
4
Suberoyl bishydroxamic acid activates notch1 signaling and suppresses tumor progression in an animal model of medullary thyroid carcinoma.辛二酰双羟肟酸在甲状腺髓样癌动物模型中激活Notch1信号通路并抑制肿瘤进展。
Ann Surg Oncol. 2008 Sep;15(9):2600-5. doi: 10.1245/s10434-008-0006-z. Epub 2008 Jun 18.
5
Valproic acid activates Notch1 signaling and induces apoptosis in medullary thyroid cancer cells.丙戊酸激活Notch1信号通路并诱导甲状腺髓样癌细胞凋亡。
Ann Surg. 2008 Jun;247(6):1036-40. doi: 10.1097/SLA.0b013e3181758d0e.
6
Current management of medullary thyroid cancer.甲状腺髓样癌的当前管理
Oncologist. 2008 May;13(5):539-47. doi: 10.1634/theoncologist.2007-0239.
7
Suberoyl bis-hydroxamic acid activates Notch-1 signaling and induces apoptosis in medullary thyroid carcinoma cells.辛二酰双羟肟酸激活Notch-1信号通路并诱导甲状腺髓样癌细胞凋亡。
Oncologist. 2008 Feb;13(2):98-104. doi: 10.1634/theoncologist.2007-0190.
8
Suberoyl bishydroxamic acid inhibits cellular proliferation by inducing cell cycle arrest in carcinoid cancer cells.辛二酰双羟肟酸通过诱导类癌癌细胞的细胞周期停滞来抑制细胞增殖。
J Gastrointest Surg. 2007 Nov;11(11):1515-20; discussion 1520. doi: 10.1007/s11605-007-0249-1. Epub 2007 Sep 15.
9
Palliation of advanced thyroid malignancies.晚期甲状腺恶性肿瘤的姑息治疗。
Surg Oncol. 2007 Dec;16(4):237-47. doi: 10.1016/j.suronc.2007.08.006. Epub 2007 Sep 14.
10
Valproic acid activates notch-1 signaling and regulates the neuroendocrine phenotype in carcinoid cancer cells.丙戊酸激活Notch-1信号通路并调节类癌癌细胞的神经内分泌表型。
Oncologist. 2007 Aug;12(8):942-51. doi: 10.1634/theoncologist.12-8-942.
Zotero 插件