The HDAC1 Knockout UM-UC-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human bladder transitional cell carcinoma line UM-UC-3, engineered for targeted disruption of the HDAC1 gene. This loss-of-function model enables investigation of class I histone deacetylase HDAC1 in cancer biology and epigenetic regulation. The polyclonal population retains the heterogeneity of the parental tumor line and is suited for pooled functional genomics and drug response assays.
The host UM-UC-3 cell line was established from a male patient with high-grade transitional cell carcinoma of the bladder and carries a mutant p53 tumor suppressor. These epithelial cells exhibit invasive carcinoma features, including rapid proliferation and migration, and are widely employed in preclinical bladder cancer research to study molecular mechanisms and test therapeutics.
HDAC1 encodes a histone deacetylase that removes acetyl groups from lysine residues on histones H3 and H4, as well as from non-histone proteins, leading to chromatin compaction and transcriptional repression. Its activity is controlled by upstream regulators such as SP1, E2F1, and PKA, and it functions within NuRD, Sin3, and CoREST complexes. HDAC1 deacetylates histone H3K9ac and H4K16ac to silence gene promoters, and also targets p53 at K382, inhibiting its transcriptional activity, while modulating E2F1, STAT3, and NF-??B. These interactions place HDAC1 at the nexus of pathways governing proliferation, apoptosis, genome stability, and signaling via Notch, Wnt, and TGF-??.
In the p53-mutant UM-UC-3 bladder cancer context, abolishing HDAC1 expression provides a system to examine p53-independent functions of this deacetylase. The knockout model allows dissection of epigenetic dependencies underlying bladder cancer cell survival, DNA repair defects, and sensitivity to genotoxic agents, offering opportunities to explore synthetic lethal interactions and identify biomarkers in a clinically relevant background.
This knockout product supports diverse research applications, including epigenetic regulation and chromatin remodeling studies, as well as gene expression analysis. It is validated for western blotting of histone and p53 acetylation, RT-qPCR, ChIP-qPCR, and functional assays such as MTT proliferation, Annexin V apoptosis, and migration/invasion assays. The model serves as a platform for HDAC inhibitor drug screening with compounds like vorinostat or valproic acid. For technical information, please contact Ascent Research.
