
PLK1-mediated phosphorylation of PHGDH reprograms serine metabolism in advanced prostate cancer.
Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to meet their increased biosynthetic and energetic demands. Although cells possess the capacity for de novo serine biosynthesis, most transformed cancer cells preferentially rely on exogenous serine uptake to sustain their growth, yet the regulatory mechanisms driving this metabolic dependency remain poorly understood. Here, we uncover a mechanism by which Polo-like kinase 1 (PLK1), frequently overexpressed in prostate cancer,
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