Emerin acts as a mechanosensor linking force transmission and disease.

For cells to respond to mechanical and biochemical cues in their environment, signals from the extracellular environment must be transmitted across the plasma membrane and into the nucleus to create the correct physical, transcriptional, and biochemical responses. This process is called mechanotransduction, which often becomes dysfunctional during cancer transformation to promote uncontrolled growth and metastatic progression. Emerin, an inner nuclear membrane (INM) protein that contributes to maintaining nuclear architecture, can receive these extracellular and extranuclear signals directly through the Linker of the Nucleoskeleton and Cytoskeleton (LINC) complex. Through association of LINC with the cytoskeleton and plasma membrane, it directly transmits force from the plasma membrane to the nucleus. Emerin has also been implicated in regulating biochemical mechanotransduction pathways, such as YAP/TAZ and MKL1/MRTFA, where emerin integrates mechanical signals with transcriptional responses. This review will discuss nuclear mechanotransduction and emerin's role as a central node that integrates mechanical signals to regulate cellular responses within complex extracellular environments, and how dysfunction contributes to cancer progression.