[Epithelial to Mesenchymal Transition Marker in 2D and 3D Colon Cancer Cell Cultures in the Presence of Laminin 332 and 411].

Received August 28, 2018; revised October 10, 2018; accepted November 6, 2018 The loss of apical-basal cell polarity is a necessary stage of the epithelial-mesenchymal transition (EMT). Polarized epithelial cells interact with the basement membrane (BM) and, in particular, with laminins, the major components of BM. Here, we examined the effect of the transition of colon cancer cells from 2D polarized state to non-polarized 3D state on the expression of EMT associated genes, as well as the role of laminins 332 and 411 (LM-332 and LM-411) in this process.

Towards embedding Caco-2 model of gut interface in a microfluidic device to enable multi-organ models for systems biology.

Background: A cancer cell line originating from human epithelial colorectal adenocarcinoma (Caco-2 cells) serves as a high capacity model for a preclinical screening of drugs. Recent need for incorporating barrier tissue into multi-organ chips calls for inclusion of Caco-2 cells into microperfused environment.

Results: This article describes a series of systems biology insights obtained from comparing Caco-2 models cells grown as conventional 2D layer and in a microfluidic chip.

Metabolic Reprogramming of Trophoblast Cells in Response to Hypoxia.

Hypoxia of trophoblast cells is an important regulator of normal development of the placenta. However, some pathological states associated with hypoxia, e.g.

Oxyquinoline-Dependent Changes in Claudin-Encoding Genes Contribute to Impairment of the Barrier Function of the Trophoblast Monolayer.

Natural response to hypoxia critically depends on rapid stabilization of hypoxia-inducible factor (HIF). Under normoxic conditions, HIF-prolyl hydroxylases mark α-subunits of HIF for degradation, while hypoxia results in stabilization of HIF-α. Oxyquinoline derivatives suppress activity of HIF-prolyl hydroxylases leading to HIF activation in the cell.