The ALDH1A2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ALDH1A2 gene in the HT29 colorectal adenocarcinoma line. This loss-of-function model eliminates retinaldehyde dehydrogenase 2 (RALDH2) activity, disrupting retinoic acid synthesis. The polyclonal format offers a heterogeneous gene-disrupted pool for studying ALDH1A2-dependent processes without clonal selection.
HT29 is a human colon carcinoma epithelial line extensively used in cancer research. These cells form polarized monolayers and retain intestinal differentiation potential, serving as a relevant model for colorectal tumor biology. The knockout derivative enables direct examination of ALDH1A2??s role in this tumorigenic epithelial context.
ALDH1A2 catalyzes the oxidation of retinaldehyde to all-trans-retinoic acid (RA), which activates nuclear receptors RAR and RXR to regulate gene transcription. Upstream regulators include Wnt/??-catenin and PAX6; downstream targets include HOX genes, CYP26A1, RAR??, and p21. Cofactor NAD+ and binding proteins CRABP1/CRABP2 modulate enzyme function. Knockout halts RA production, decoupling this signaling cascade.
In HT29 cells, ALDH1A2 knockout impairs RA-mediated differentiation and apoptosis, potentially promoting tumorigenic traits. The model allows dissection of RA??s tumor-suppressive effects, often antagonized by oncogenic Wnt/??-catenin signaling in colorectal cancer. The polyclonal population reflects clonal heterogeneity typical of tumors, enabling studies of differential responses.
Applications include exploring retinoic acid signaling in colorectal cancer, differentiation therapy, and retinol metabolism. Assays such as LC-MS for RA measurement, RA-responsive reporters, qPCR for target genes (e.g., HOX genes, CYP26A1), flow cytometry for differentiation markers, and proliferation/invasion assays are compatible. For more information, contact Ascent Research.
