MCF-7

MCF-7 is a breast cancer cell line. ^[1] MCF-7 is the acronym of Michigan Cancer Foundation-7, referring to the institute in Detroit where the cell line was established in 1973 by Herbert Soule and co-workers.^[2] The Michigan Cancer Foundation is now known as the Barbara Ann Karmanos Cancer Institute.^[3]

MCF-7 cells

MCF-7 and two other breast cancer cell lines, named T-47D and MDA-MB-231, account for more than two-thirds of all abstracts reporting studies on mentioned breast cancer cell lines, as concluded from a Medline-based survey.^[4]

Isolation

MCF-7 was isolated in 1970 from a 69-year-old woman. ^[1] The patient, Frances Mallon died in 1970 due to metastatic breast cancer.^[5] Her cells were the source of much of current knowledge about breast cancer.^[2][6]

Prior to MCF-7, it was not possible for cancer researchers to obtain a mammary cell line that was capable of living longer than a few months.^[7]

Uses

MCF-7 has potential for new drug development, including anti-cancer drug testing, anti-estrogen drug resistance and antiplatelet drug development.^[8]

Antiproliferation

Tumor necrosis factor alpha (TNF alpha) inhibits the growth of MCF-7 breast cancer cells. Treatment with anti-estrogens can modulate the secretion of insulin-like growth factor binding proteins. Omega-3 and 6 fatty acids such as EPA, DHA and AA has been reported to inhibit MCF-7 cell line growth and proliferation.^[9]

Many studies indicate that the insulin-like growth factor 1 receptor is a crucial therapeutic target for treating cancer in MCF-7 cell lines.^[10] One notably effective treatment strategy is silencing this receptor using siRNA packaged in nanoparticles, which significantly suppresses the growth and proliferation of MCF-7 cancer cells.^[11]

The results of IC₅₀ determination (Liu et al.) of compounds of Melilotus officinalis (Linn.) Pall. were published during 2018. ^[12]

Tamoxifen increases FasL and TNF-α. ^[13]

Characteristics of MCF-7 cells

MCF-7 cells have the following characteristics:^{[2][6][4][14][15][16]}

• Primary tumor (invasive breast ductal carcinoma)
• Originate from pleural effusion
• 17β-estradiol ^[17] receptors present ^[8]
• Proliferative response to estrogens
• Presence of progesterone receptors
• Contains 17β-estradiol-binding protein^[8]
• Cannot have ERBB2 gene amplification (with Her2/neu protein overexpression)
• Tumorigenic in mice but only with estrogen supplementation if engrafted into the subcutaneous fat or mammary fat pad
• Tumorigenic in mice without estrogen supplementation if engrafted intraductally^[18]
• Luminal epithelial phenotype
• PIK3CA helical mutations were identified in MCF-7,^[19] but with low AKT activation.^[20]

This cell line retained several characteristics of differentiated mammary epithelium, including the ability to process estradiol via cytoplasmic estrogen receptors and the capability of forming domes.^{[citation needed]}