3D in vitro models of tumors expressing EGFR family receptors: a potent tool for studying receptor biology and targeted drug development. Issue 1 (January 2019)

• Record Type: Journal Article
• Authors: Sokolova, Evgeniya A.; Vodeneev, Vladimir A.; Deyev, Sergey M.; Balalaeva, Irina V.
• Is Part Of: Drug discovery today. Volume 24:Issue 1(2019)
• Page Start: 99
• Page End: 111
• Publication Date: 2019-01
• Subjects: Drugs -- Design -- Periodicals; Drugs -- Research -- Periodicals; 615.1
• DOI: 10.1016/j.drudis.2018.09.003
• Languages: English
• ISSNs: 1359-6446

Abstract

Graphical abstract: Highlights: High mortality from tumors expressing EGFR family receptors remains a serious problem. The biology of EGFR (HER) family receptors is affected by 3D organization of tumor tissue. 3D organization often leads to tumor cell resistance to targeted anti-HER drugs. Use of advanced in vitro tumor models can facilitate targeted drug development. Abstract : Carcinomas overexpressing EGFR family receptors are of high clinical importance, because the receptors have prognostic value and are used as molecular targets for anticancer therapy. Insufficient drug efficacy necessitates further in-depth research of the receptor biology and improvement in preclinical stages of drug evaluation. Here, we review the currently used advanced 3D in vitro models of tumors, including tumor spheroids, models in natural and synthetic matrices, tumor organoids and microfluidic-based models, as a potent tool for studying EGFR biology and targeted drug development. We are especially focused on factors that affect the biology of tumor cells, causing modification in the expression and basic phosphorylation of the receptors, crosstalk with other signaling pathways and switch between downstream cascades, resulting ultimately in the resistance to antitumor agents. Teaser: This review highlights currently used 3D in vitro models of tumors expressing EGFR family receptors with special focus on factors affecting tumor cell biology and resistance to antitumor agents.