The ALDH1B1 Knockout UM-UC-3 Polyclonal Cells product comprises a population of UM-UC-3 human bladder carcinoma cells that have been subjected to CRISPR/Cas9-mediated gene editing to disrupt the ALDH1B1 locus. This polyclonal knockout cell population is designed for loss-of-function studies of aldehyde dehydrogenase 1 family member B1 (ALDH1B1) in a bladder cancer context. The heterogeneous nature of the polyclonal pool reflects the varying editing outcomes across individual cells, providing a robust model to investigate gene function without the constraints of a single clonal genotype.
The host UM-UC-3 cell line is a widely utilized model of human bladder transitional cell carcinoma, originally established from a male patient. These epithelial cells retain key characteristics of high-grade bladder cancer, including invasive potential and tumorigenicity, making them suitable for studying molecular mechanisms underlying bladder cancer progression.
ALDH1B1 encodes a mitochondrial aldehyde dehydrogenase that catalyzes the NAD+-dependent oxidation of retinaldehyde to retinoic acid, a critical morphogen. This enzyme functions within the retinoid signaling axis, linking retinol metabolism to transcriptional regulation via retinoic acid receptors (RARs) and retinoid X receptors (RXRs). ALDH1B1 expression is transcriptionally regulated by the ??-catenin/TCF complex downstream of WNT ligands, integrating developmental and oncogenic signals. In addition to its biosynthetic role, ALDH1B1 contributes to cellular detoxification by oxidizing lipid peroxidation-derived aldehydes. The enzyme is known to interact with NAD+ as a cofactor and may form heterotetramers with other ALDH isoforms, although its functional partners remain under investigation.
Disruption of ALDH1B1 in UM-UC-3 bladder cancer cells is expected to impair retinaldehyde-to-retinoic acid conversion, leading to attenuated RAR/RXR-mediated transcription. Given the enzyme’s association with cancer stem cell maintenance and the stemness phenotype characterized by markers such as CD44 and OCT4, this knockout model offers a valuable tool to dissect the role of retinoid signaling in bladder tumor biology. The polyclonal knockout population provides a physiologically relevant system to assess how heterogeneous ALDH1B1 loss influences tumorigenic potential, self-renewal, and the response to ALDH-targeted therapies.
This ALDH1B1 knockout cell product is suited for a range of experimental workflows, including functional genomics screens, retinoic acid pathway interrogation, and drug target validation in bladder cancer. Researchers can employ ALDH enzymatic activity assays or Aldefluor flow cytometry to confirm loss of ALDH function, while Western blotting for stemness markers such as CD44 and OCT4 can evaluate impact on the cancer stem cell phenotype. Migration and invasion assays enable assessment of metastatic behavior, and drug sensitivity studies may reveal synthetic lethal interactions or resistance mechanisms. Additionally, RNA-seq transcriptome analysis can provide a global view of gene expression changes induced by ALDH1B1 disruption. For further details or to request a quote, please contact Ascent Research.
