John Maringa Githaka

Abstract Metabolic dysfunction-associated steatohepatitis (MASH) and metabolic dysfunction-associated steatotic liver disease (MASLD) develop because of fat disposition and excess accumulation of lipid droplets in hepatocytes and hepatic stellate cells. The endoplasmic reticulum enzyme stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme that converts saturated fatty acids (SFAs) to monounsaturated fatty acids (MUFAs).

arising from X. Zhang et al. Communications Medicine https://doi.org/10.1038/s43856-022-00142-3 (2022) Therapies that induce apoptosis in cancer cells are critically important in clinical oncology. In a recent Communications Medicine article1 and Proceedings of the National Academy of Sciences article2, a small molecule, NPB, was reported to induce cancer cell-specific cell death by inhibiting phosphorylation of the apoptotic protein, BAD.

Abstract The Bcl-2 family member BAD is a candidate disease modulator because it stimulates apoptosis in a cell context basis and inhibits cell migration during normal mammary gland morphogenesis. This activity depends on 3 key regulatory serines (S75, 99, 118) in the unphosphorylated state. Given that developmental programs are often hijacked in cancer, we hypothesized that BAD would impede breast cancer progression.