The epithelial polarity axis controls the resting membrane potential and Cl- co-transport in breast glandular structures.

The membrane potential (MP) controls cell homeostasis by directing molecule transport and gene expression. How the MP is set upon epithelial differentiation is unknown. Given that tissue architecture also controls homeostasis, we investigated the relationship between basoapical polarity and resting MP in three-dimensional culture of the HMT-3522 breast cancer progression.

Organ-on-a-Chip Platform with an Integrated Screen-Printed Electrode Array for Real-Time Monitoring Trans-Epithelial Barrier and Bubble Formation.

Cellular tight junctions play a key role in establishing a barrier between different compartments of the body by regulating the selective passage of different solutes across epithelial and endothelial tissues. Over the past decade, significant efforts have been conducted to develop more clinically relevant "organ-on-a-chip" models with integrated trans-epithelial electrical resistance (TEER) monitoring systems to help better understand the fundamental underpinnings of epithelial tissue physiology upon exposure to different substances. However, most of these platforms require the use of high-cost and time-consuming photolithography processes, which limits their scalability and practical implementation in clinical research.

Over-expression of miR-183-5p or miR-492 triggers invasion and proliferation and loss of polarity in non-neoplastic breast epithelium.

microRNAs (miRNAs) serve as novel noninvasive cancer biomarkers. In an HMT-3522 S1 (S1) breast epithelial risk-progression three-dimensional (3D) culture model, non-neoplastic S1 cells form a fully polarized epithelium. When silenced for the gap junction and tumor suppressor Cx43, Cx43-KO-S1 cells recapitulate pre-neoplastic phenotypes observed in tissues at risk for breast cancer in vivo.

Embedding the Community and Individuals in Disease Prevention.

The primary prevention of non-communicable diseases is one of the most challenging and exciting aspects of medicine and primary care this century. For cancer, it is an urgent matter in light of the increasing burden of the disease among younger people and the higher frequency of more aggressive forms of the disease for all ages. Most chronic disorders result from the influence of the environment on the expression of genes within an individual.

Can the epigenome contribute to risk stratification for cancer onset?

The increasing burden of cancer requires identifying and protecting individuals at highest risk. The epigenome provides an indispensable complement to genetic alterations for a risk stratification approach for the following reasons: gene transcription necessary for cancer onset is directed by epigenetic modifications and many risk factors studied so far have been associated with alterations related to the epigenome. The risk level depends on the plasticity of the epigenome during phases of life particularly sensitive to environmental and dietary impacts.