Context-dependent effects of DHRS2 on cell-cycle progression, apoptosis and inflammatory gene expression in breast cell lines

Silencing DHRS2 disrupted pathways such as ribosome biogenesis, DNA replication, and ion transport, whereas overexpression altered mitochondrial gene transcription and nucleoside synthesis. Loss of DHRS2 accelerated cell-cycle progression in MCF-7 and MCF-10A cells, whereas its overexpression induced G0/G1 phase arrest.

Apoptosis levels increased with knockdown and decreased with overexpression, mainly in cancer cells. Inflammatory gene responses varied depending on cell type, particularly involving CASP1, IL-1A/B, and PYHIN1. Overexpression of DHRS2 promoted cell detachment and migration, suggesting cytoskeletal remodeling.