HSP90 Inhibition and Cellular Stress Elicits Phenotypic Plasticity in Hematopoietic Differentiation

The study investigated the role of HSP90 inhibition in promoting phenotypic plasticity in hematopoietic differentiation using EML cells. It found that inhibiting HSP90 with geldanamycin increased cellular plasticity and survival under stress, suggesting HSP90's role in canalization and plasticity. This plasticity involved epigenetic mechanisms, particularly histone acetylation, and required high levels of stem cell factor signaling. The study concluded that HSP90 inhibition enhanced phenotypic plasticity without altering proliferation rates or cell differentiation markers, highlighting HSP90 as a potential target for influencing cellular differentiation and plasticity, with implications for cancer progression and regenerative medicine. However, the findings were limited to a single noncancerous cell line, indicating the need for further research.