Why the study?
The adaptation of lipid metabolism in cancer cells, driven by microenvironmental changes, presents major challenges for cancer therapy.
Population
Cancer cells in vitro and in vivo tumor models
Comparison
SCD1 knockdown or pharmacological inhibition vs control
Design
Preclinical in vitro and in vivo study
Key result
Knockdown or pharmacological inhibition of SCD1 enhanced cancer cell sensitivity to HDAC inhibitors by reshaping the cellular acetylome and destabilizing nucleophosmin-1.
Authors
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SCD1 inhibition may enhance HDAC inhibitor sensitivity in cancer cells; leaves open clinical translation and patient outcomes.
Targeting SCD1 could sensitize cancer cells to HDAC inhibitors by reshaping the cellular acetylome.
Wéry et al. (2026) studied Cancer. SCD1 knockdown or pharmacological inhibition was evaluated on Tumor growth, cell proliferation, and sensitivity to HDAC inhibitors. Knockdown or pharmacological inhibition of SCD1 enhanced cancer cell sensitivity to HDAC inhibitors by reshaping the cellular acetylome and destabilizing nucleophosmin-1.