MDA-MB231

'''MDA-MB-231''' (M D Anderson - Metastatic Breast - 231) is a human breast cancer cell line isolated at MD Anderson Cancer Center in 1973 that is used in therapeutic research, especially in the context of triple negative breast cancer.<ref>{{cite journal | vauthors = Cailleau R, Young R, Olivé M, Reeves WJ | title = Breast tumor cell lines from pleural effusions | journal = Journal of the National Cancer Institute | volume = 53 | issue = 3 | pages = 661–674 | date = September 1974 | pmid = 4412247 | pmc = 7364228 | doi = 10.1093/jnci/53.3.661 }}</ref><ref name=":0">{{Cite web |date=January 30, 2024 |title=Cellosaurus MDA-MB-231 (CVCL_0062) |url=https://www.cellosaurus.org/CVCL_0062 |website=Cellosaurus}}</ref>

== History and characteristics == MDA-MB-231 cells were derived from a pleural effusion due to an adenocarcinoma originating in a 51-year-old caucasian female.<ref name=":0" /> The cell line is triple negative, meaning it lacks oestrogen receptors, progesterone receptors, and HER2 (human epidermal growth factor receptor 2) amplification which many current treatment options rely on making it difficult to cure.<ref>{{cite journal | vauthors = Liu H, Zang C, Fenner MH, Possinger K, Elstner E | title = PPARgamma ligands and ATRA inhibit the invasion of human breast cancer cells in vitro | journal = Breast Cancer Research and Treatment | volume = 79 | issue = 1 | pages = 63–74 | date = May 2003 | pmid = 12779083 | doi = 10.1023/a:1023366117157 | s2cid = 25517953 }}</ref><ref>{{cite journal | vauthors = Chavez KJ, Garimella SV, Lipkowitz S | title = Triple negative breast cancer cell lines: one tool in the search for better treatment of triple negative breast cancer | journal = Breast Disease | volume = 32 | issue = 1–2 | pages = 35–48 | date = 2010 | pmid = 21778573 | pmc = 3532890 | doi = 10.3233/BD-2010-0307 }}</ref> In addition, this cell line has a low expression of the Ki-67 proliferation marker, down regulation of claudin-3 and claudin-4, enrichment for markers associated with the epithelial-mesenchymal transition and the CD44+CD24-/low phenotype associated with breast cancer stem cells and increased metastasis,<ref>{{cite journal | vauthors = Holliday DL, Speirs V | title = Choosing the right cell line for breast cancer research | journal = Breast Cancer Research | volume = 13 | issue = 4 | pages = 215 | date = August 2011 | pmid = 21884641 | pmc = 3236329 | doi = 10.1186/bcr2889 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Prat A, Parker JS, Karginova O, Fan C, Livasy C, Herschkowitz JI, He X, Perou CM | title = Phenotypic and molecular characterization of the claudin-low intrinsic subtype of breast cancer | journal = Breast Cancer Research | volume = 12 | issue = 5 | pages = R68 | date = 2010 | pmid = 20813035 | pmc = 3096954 | doi = 10.1186/bcr2635 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Gowrikumar S, Singh AB, Dhawan P | title = Role of Claudin Proteins in Regulating Cancer Stem Cells and Chemoresistance-Potential Implication in Disease Prognosis and Therapy | journal = International Journal of Molecular Sciences | volume = 21 | issue = 1 | pages = 53 | date = December 2019 | pmid = 31861759 | pmc = 6982342 | doi = 10.3390/ijms21010053 | doi-access = free }}</ref> and is a mutant in the p53 and KRas oncogenes.<ref>{{cite journal | vauthors = Hollestelle A, Nagel JH, Smid M, Lam S, Elstrodt F, Wasielewski M, Ng SS, French PJ, Peeters JK, Rozendaal MJ, Riaz M, Koopman DG, Ten Hagen TL, de Leeuw BH, Zwarthoff EC, Teunisse A, van der Spek PJ, Klijn JG, Dinjens WN, Ethier SP, Clevers H, Jochemsen AG, den Bakker MA, Foekens JA, Martens JW, Schutte M | title = Distinct gene mutation profiles among luminal-type and basal-type breast cancer cell lines | journal = Breast Cancer Research and Treatment | volume = 121 | issue = 1 | pages = 53–64 | date = May 2010 | pmid = 19593635 | doi = 10.1007/s10549-009-0460-8 | s2cid = 22587331 | url = https://hal.archives-ouvertes.fr/hal-00485063/file/PEER_stage2_10.1007%252Fs10549-009-0460-8.pdf }}</ref><ref>{{cite journal | vauthors = Kim RK, Suh Y, Yoo KC, Cui YH, Kim H, Kim MJ, Gyu Kim I, Lee SJ | title = Activation of KRAS promotes the mesenchymal features of basal-type breast cancer | journal = Experimental & Molecular Medicine | volume = 47 | issue = 1 | pages = e137 | date = January 2015 | pmid = 25633745 | pmc = 4314588 | doi = 10.1038/emm.2014.99 }}</ref> The cells are considered biosafety level 1. They can be grown in 2 or 3-D cultures.<ref>{{cite journal | vauthors = Huang Z, Yu P, Tang J | title = Characterization of Triple-Negative Breast Cancer MDA-MB-231 Cell Spheroid Model | journal = OncoTargets and Therapy | volume = 13 | pages = 5395–5405 | date = 2020-06-11 | pmid = 32606757 | pmc = 7295545 | doi = 10.2147/OTT.S249756 | doi-access = free }}</ref>

== Research applications == MDA-MB-231 is used to study potential treatments for a cancer with currently limited treatment options by either improving current medication delivery and efficacy,<ref>{{cite journal | vauthors = Mohammed F, Rashid-Doubell F, Taha S, Cassidy S, Fredericks S | title = Effects of curcumin complexes on MDA‑MB‑231 breast cancer cell proliferation | journal = International Journal of Oncology | volume = 57 | issue = 2 | pages = 445–455 | date = August 2020 | pmid = 32626932 | pmc = 7307592 | doi = 10.3892/ijo.2020.5065 }}</ref><ref>{{cite journal | vauthors = Raut J, Sarkar O, Das T, Mandal SM, Chattopadhyay A, Sahoo P | title = Efficient delivery of methotrexate to MDA-MB-231 breast cancer cells by a pH-responsive ZnO nanocarrier | journal = Scientific Reports | volume = 13 | issue = 1 | pages = 21899 | date = December 2023 | pmid = 38081993 | pmc = 10713526 | doi = 10.1038/s41598-023-49464-9 | bibcode = 2023NatSR..1321899R }}</ref> or by trying new treatment courses.<ref>{{cite journal | vauthors = Liu S, Dong Y, Wang Y, Hu P, Wang J, Wang RY | title = Pristimerin exerts antitumor activity against MDA-MB-231 triple-negative breast cancer cells by reversing of epithelial-mesenchymal transition via downregulation of integrin β3 | journal = Biomedical Journal | volume = 44 | issue = 6 Suppl 1 | pages = S84–S92 | date = December 2021 | pmid = 35652598 | pmc = 9038948 | doi = 10.1016/j.bj.2020.07.004 }}</ref><ref>{{cite journal | vauthors = Govindaraj S, Ganesan K, Dharmasivam M, Raman L, Alam MM, Amanullah M | title = Synthesis of potent MDA-MB 231 breast cancer drug molecules from single step | journal = Scientific Reports | volume = 13 | issue = 1 | pages = 18241 | date = October 2023 | pmid = 37880270 | pmc = 10600176 | doi = 10.1038/s41598-023-45455-y | bibcode = 2023NatSR..1318241G }}</ref>

This cell line has also been utilized to study metastasis to the bones<ref>{{cite journal | vauthors = Wright LE, Ottewell PD, Rucci N, Peyruchaud O, Pagnotti GM, Chiechi A, Buijs JT, Sterling JA | title = Murine models of breast cancer bone metastasis | journal = BoneKEy Reports | volume = 5 | pages = 804 | date = 2016 | pmid = 27867497 | pmc = 5108088 | doi = 10.1038/bonekey.2016.31 }}</ref><ref name=":1">{{cite journal | vauthors = Jekabsons MB, Merrell M, Skubiz AG, Thornton N, Milasta S, Green D, Chen T, Wang YH, Avula B, Khan IA, Zhou YD | title = Breast cancer cells that preferentially metastasize to lung or bone are more glycolytic, synthesize serine at greater rates, and consume less ATP and NADPH than parent MDA-MB-231 cells | journal = Cancer & Metabolism | volume = 11 | issue = 1 | pages = 4 | date = February 2023 | pmid = 36805760 | pmc = 9940388 | doi = 10.1186/s40170-023-00303-5 | doi-access = free }}</ref> and lungs.<ref name=":1" /><ref>{{cite journal | vauthors = Minn AJ, Gupta GP, Siegel PM, Bos PD, Shu W, Giri DD, Viale A, Olshen AB, Gerald WL, Massagué J | title = Genes that mediate breast cancer metastasis to lung | journal = Nature | volume = 436 | issue = 7050 | pages = 518–524 | date = July 2005 | pmid = 16049480 | pmc = 1283098 | doi = 10.1038/nature03799 | bibcode = 2005Natur.436..518M }}</ref>

== See also == * List of breast cancer cell lines

== References == {{Reflist}}

Category:Human cell lines Category:Breast cancer cell lines