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MCF-7

维基百科,自由的百科全书
MCF-7 细胞

MCF-7Michigan Cancer Foundation-7)是一种乳腺癌细胞系[1],最初在1970年分离自一名69岁的白人女性乳腺癌患者弗朗西丝·马隆(Frances Mallon)。MCF-7是密歇根州癌症基金会-7(Michigan Cancer Foundation-7,现称卡马诺斯癌症研究所英语Karmanos Cancer Institute)的首字母缩写,指的是赫伯特·苏尔(Herbert Soule)及其同事在一间位于底特律研究所建立此细胞系[2]。在建立MCF-7细胞之前,癌症研究人员不可能获得能够存活超过几个月的乳腺癌细胞系[3]。1970年,一位名为弗朗西丝·马隆的修女去世,而从她身上获得的细胞是当前许多有关乳腺癌的知识的来源[2][4]。除此之外,利用MEDLINE书目资料库进行调查后,发现三分之二的乳腺癌细胞系研究的摘要中都有MCF-7和另外两个乳腺癌细胞系T-47DMDA-MB-231[5]

特征

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综合多份文献,MCF-7细胞具有以下特征[2][4][5][6][7][8]:它是一种源自胸腔积液的浸润性乳腺导管癌的细胞系,具有苯巴比妥能上皮表型(Luminal epithelial phenotype),并且表达孕酮受体雌激素受体英语Estrogen receptor。具有过度表达的HER2/neu蛋白,同时又不具有ERBB2基因的扩增。当存在雌激素时,MCF-7细胞就会增殖。此外,MCF-7细胞在小鼠中具有致瘤性,但是仅当植入皮下脂肪或乳腺脂肪垫英语Fat pad中时,才须要补充雌激素。如果是导管内植入,则在未补充雌激素的小鼠中具有致瘤性[9]

该细胞系保留了已经历细胞分化的乳腺上皮组织的几个特征,包括通过细胞质雌激素受体加工雌二醇的能力,以及形成穹顶(domes)的能力。目前已知肿瘤坏死因子-α可以抑制MCF-7细胞的生长,并且在治疗期间使用抗雌激素,可以调节胰岛素样生长因子结合蛋白分泌。有研究指出ω-3脂肪酸和6种脂肪酸(例如二十碳五烯酸二十二碳六烯酸花生四烯酸)可以抑制MCF-7细胞的生长和增殖[10]。除此之外,有部分研究发现MCF-7细胞中具有PIK3CA英语P110α螺旋突变,以及蛋白激酶B(AKT)激活率较低的现象[11]

参考资料

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  1. ^ Lee, Adrian V.; et al. MCF-7 Cells—Changing the Course of Breast Cancer Research and Care for 45 Years. Journal of the National Cancer Institute. 1 July 2015, 107 (7): djv073. PMID 25828948. doi:10.1093/jnci/djv073. 
  2. ^ 2.0 2.1 2.2 Soule, HD; Vazquez J; Long A; Albert S; Brennan M. A human cell line from a pleural effusion derived from a breast carcinoma. Journal of the National Cancer Institute. 1973, 51 (5): 1409–1416. PMID 4357757. doi:10.1093/jnci/51.5.1409. 
  3. ^ Glodek, Cass, Ph.D., "A History of the Michigan Cancer Foundation, the Beginnings & Growth of Detroit's Anticancer Movement," 1990, page 68, Michigan Cancer Foundation, Detroit.
  4. ^ 4.0 4.1 Levenson, AS; Jordan VC. MCF-7: the first hormone-responsive breast cancer cell line. Cancer Research. 1997, 57 (15): 3071–3078. PMID 9242427. 
  5. ^ 5.0 5.1 Lacroix, M; Leclercq G. Relevance of breast cancer cell lines as models for breast tumours: an update. Breast Research and Treatment. 2004, 83 (3): 249–289. PMID 14758095. doi:10.1023/B:BREA.0000014042.54925.cc. 
  6. ^ Ross, DT; Perou CM. A comparison of gene expression signatures from breast tumors and breast tissue derived cell lines. Disease Markers. 2001, 17 (2): 99–109. PMC 3850857可免费查阅. PMID 11673656. doi:10.1155/2001/850531. 
  7. ^ Charafe-Jauffret, E; Ginestier C; Monville F; Finetti P; Adelaide J; Cervera N; Fekairi S; Xerri L; Jacquemier J; Birnbaum D; Bertucci F. Gene expression profiling of breast cell lines identifies potential new basal markers. Oncogene. 2006, 25 (15): 2273–2284. PMID 16288205. doi:10.1038/sj.onc.1209254. 
  8. ^ Lacroix, M; Toillon RA; Leclercq G. p53 and breast cancer, an update. Endocrine-Related Cancer (Bioscientifica). 2006, 13 (2): 293–325. PMID 16728565. doi:10.1677/erc.1.01172. 
  9. ^ Sflomos, George; Dormoy, Valerian; Metsalu, Tauno; Jeitziner, Rachel; Battista, Laura; Scabia, Valentina; Raffoul, Wassim; Delaloye, Jean-Francois; Treboux, Assya. A Preclinical Model for ERα-Positive Breast Cancer Points to the Epithelial Microenvironment as Determinant of Luminal Phenotype and Hormone Response. Cancer Cell. 2016, 29 (3): 407–422. PMID 26947176. doi:10.1016/j.ccell.2016.02.002. 
  10. ^ Mansara, Prakash P.; Deshpande, Rashmi A.; Vaidya, Milind M.; Kaul-Ghanekar, Ruchika. Differential Ratios of Omega Fatty Acids (AA/EPA+DHA) Modulate Growth, Lipid Peroxidation and Expression of Tumor Regulatory MARBPs in Breast Cancer Cell Lines MCF7 and MDA-MB-231. PLOS ONE. 1 September 2015, 10 (9): e0136542. ISSN 1932-6203. PMC 4556657可免费查阅. PMID 26325577. doi:10.1371/journal.pone.0136542. 
  11. ^ Vasudevan, Krishna M.; Barbie, David A.; Davies, Michael A.; Rabinovsky, Rosalia; McNear, Chontelle J.; Kim, Jessica J.; Hennessy, Bryan T.; Tseng, Hsiuyi; Pochanard, Panisa. AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancer. Cancer Cell. 2009-07-07, 16 (1): 21–32. ISSN 1878-3686. PMC 2752826可免费查阅. PMID 19573809. doi:10.1016/j.ccr.2009.04.012. 

外部链接

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