NSDHL (NAD(P) dependent 3-beta-hydroxysteroid dehydrogenase) is an X-linked enzyme essential for post-squalene cholesterol biosynthesis, catalyzing the NAD(P)-dependent oxidative decarboxylation of C4 methyl groups in 4-alpha-carboxysterols 1. Beyond its enzymatic role, NSDHL regulates EGFR trafficking and signaling 2. Loss-of-function NSDHL mutations cause CHILD syndrome (congenital hemidysplasia with ichthyosiform erythroderma and limb defects), an X-linked dominant condition typically lethal in males 13. Female carriers present with unilateral ichthyosiform erythroderma and ipsilateral limb abnormalities 45. Clinically, NSDHL dysfunction has emerged as oncologically significant. In pancreatic ductal adenocarcinoma, NSDHL inhibition or cholesterol depletion triggers TGF-Ξ²/epithelial-mesenchymal transition signaling, promoting a basal mesenchymal phenotype associated with poor prognosis 6. Similarly, NSDHL maintains breast cancer stem-like cells through TGF-Ξ²/Smad signaling, with knockdown suppressing tumor-initiating capacity 7. In bladder cancer, the USP43/E2F1/NSDHL pathway regulates cholesterol homeostasis to promote gemcitabine resistance 8. These findings establish NSDHL as a dual-function protein with critical roles in metabolic regulation and cancer stem cell maintenance, positioning it as a therapeutic target for multiple malignancies.
No tissue expression data available for this gene.