Figure 3.

Shifting the activation curve of mechanoresponsive proteins and their partners is a viable strategy for developing cancer therapeutics. Cancer progression and tumor formation is marked by altered expression in the mechanoresponsive proteins, α-actinin, filamin, and nonmuscle myosin II (NMII), as well as partnering proteins such as 14-3-3 and CLP36. Left unchecked, the altered in gene expression correlate with increased cell activity, specifically metastasis. Because mechanoresponsive proteins such as NMIIs also have tumor-suppressive roles as they inhibit pathways such as the ERK pathway, pharmacological inhibition can lead to enhanced tumor growth. In contrast, activators can lock in a cell, leading to anticancer behaviors. One such example is the activator 4-HAP, which increases nonmuscle myosin IIB and IIC assembly, leading to increased cortical tension and reduced tumor metastatic activity. Figure created with BioRender.com. 4-HAP, 4-hydroxyacetophenone.