A microfluidic mammary gland coculture model using parallel 3D lumens for studying epithelial-endothelial migration in breast cancer.

In breast cancer development, crosstalk between mammary epithelial cells and neighboring vascular endothelial cells is critical to understanding tumor progression and metastasis, but the mechanisms of this dynamic interplay are not fully understood. Current cell culture platforms do not accurately recapitulate the 3D luminal architecture of mammary gland elements. Here, we present the development of an accessible and scalable microfluidic coculture system that incorporates two parallel 3D luminal structures that mimic vascular endothelial and mammary epithelial cell layers, respectively.

Microfluidic platform for studying osteocyte mechanoregulation of breast cancer bone metastasis.

Bone metastasis is a common, yet serious, complication of breast cancer. Breast cancer cells that extravasate from blood vessels to the bone devastate bone quality by interacting with bone cells and disrupting the bone remodeling balance. Although exercise is often suggested as a cancer intervention strategy and mechanical loading during exercise is known to regulate bone remodeling, its role in preventing bone metastasis remains unknown.

Modelling of endothelial cell migration and angiogenesis in microfluidic cell culture systems.

Tumour-induced angiogenesis is a complex biological process that involves growth of new blood vessels within the tumour microenvironment and is an important target for cancer therapies. Significant efforts have been undertaken to develop theoretical models as well as in vitro experimental models to study angiogenesis in a highly controllable and accessible manner. Various mathematical models have been developed to study angiogenesis, but these have mostly been applied to in vivo assays.

Herpes simplex virus internalization into epithelial cells requires Na+/H+ exchangers and p21-activated kinases but neither clathrin- nor caveolin-mediated endocytosis.

Unlabelled: Herpes simplex virus 1 (HSV-1) is an alphaherpesvirus that has been reported to infect some epithelial cell types by fusion at the plasma membrane but others by endocytosis. To determine the molecular mechanisms of productive HSV-1 cell entry, we perturbed key endocytosis host factors using specific inhibitors, RNA interference (RNAi), or overexpression of dominant negative proteins and investigated their effects on HSV-1 infection in the permissive epithelial cell lines Vero, HeLa, HEp-2, and PtK2. HSV-1 internalization required neither endosomal acidification nor clathrin- or caveolin-mediated endocytosis.