MCF-7Michigan Cancer Foundation-7)是一種乳腺癌細胞系[1],最初在1970年分離自一名69歲的白人女性乳腺癌患者弗朗西絲·馬隆(Frances Mallon)。MCF-7是密西根州癌症基金會-7(Michigan Cancer Foundation-7,現稱卡馬諾斯癌症研究所英語Karmanos Cancer Institute)的首字母縮寫,指的是赫伯特·蘇爾(Herbert Soule)及其同事在一間位於底特律研究所建立此細胞系[2]。在建立MCF-7細胞之前,癌症研究人員不可能獲得能夠存活超過幾個月的乳腺癌細胞系[3]。1970年,一位名為弗朗西絲·馬隆的修女去世,而從她身上獲得的細胞是當前許多有關乳腺癌的知識的來源[2][4]。除此之外,利用MEDLINE書目資料庫進行調查後,發現三分之二的乳腺癌細胞系研究的摘要中都有MCF-7和另外兩個乳腺癌細胞系T-47DMDA-MB-231[5]

MCF-7 細胞

特徵

編輯

綜合多份文獻,MCF-7細胞具有以下特徵[2][4][5][6][7][8]:它是一種源自胸腔積液的浸潤性乳腺導管癌的細胞系,具有苯巴比妥能上皮表型(Luminal epithelial phenotype),並且表達孕酮受體雌激素受體英語Estrogen receptor。具有過度表達的HER2/neu蛋白,同時又不具有ERBB2基因的擴增。當存在雌激素時,MCF-7細胞就會增殖。此外,MCF-7細胞在小鼠中具有致瘤性,但是僅當植入皮下脂肪或乳腺脂肪墊英語Fat pad中時,才須要補充雌激素。如果是導管內植入,則在未補充雌激素的小鼠中具有致瘤性[9]

該細胞系保留了已經歷細胞分化的乳腺上皮組織的幾個特徵,包括通過細胞質雌激素受體加工雌二醇的能力,以及形成穹頂(domes)的能力。目前已知腫瘤壞死因子-α可以抑制MCF-7細胞的生長,並且在治療期間使用抗雌激素,可以調節胰島素樣生長因子結合蛋白分泌。有研究指出ω-3脂肪酸和6種脂肪酸(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細胞的生長和增殖[10]。除此之外,有部分研究發現MCF-7細胞中具有PIK3CA英語P110α螺旋突變,以及蛋白激酶B(AKT)激活率較低的現象[11]

參考資料

編輯
  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 . 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 . 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 . PMID 19573809. doi:10.1016/j.ccr.2009.04.012. 

外部連結

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