HNRNPAB Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population created by disrupting the HNRNPAB gene in the HT29 colorectal adenocarcinoma cell line. This pooled knockout model provides a loss-of-function platform to investigate HNRNPAB-dependent RNA processing and gene regulation in a bulk cell population context, avoiding clonal artifacts.
The parental HT29 line, derived from a primary colorectal adenocarcinoma of a 44-year-old Caucasian female, is an adherent epithelial cell line with mutant TP53 and wild-type KRAS. HT29 is widely used as a model for colorectal cancer research, including studies of epithelial barrier function, differentiation, and tumorigenesis, and it is responsive to diverse pharmacological challenges.
HNRNPAB is a multifunctional RNA-binding protein that governs pre-mRNA splicing, mRNA stability, transport, and translation. It functions within MYC- and p53-centered regulatory circuits: it is transcriptionally activated by MYC, regulated by DNA damage and MAPK signaling, and modulated by SUMOylation. HNRNPAB directly controls the expression of key effectors such as MYC, BCL2, CDKN1A (p21), MMP13, and miR-21, thereby influencing proliferation and apoptosis. It forms interactions with YBX1, hnRNP K, TARDBP, spliceosomal components, and RNA polymerase II to carry out its post-transcriptional functions, bridging the p53-MDM2-BAX apoptotic axis and the MYC network.
Because HT29 cells harbor a TP53 mutation, the HNRNPAB knockout allows dissection of p53-independent gene regulatory mechanisms that impact colorectal cancer cell fate. Loss of HNRNPAB in this background can reveal its role in maintaining the malignant transcriptome, including altered isoform profiles and deregulated target expression, and can help unravel how post-transcriptional control contributes to drug responses and tumor cell plasticity.
Applications include Western blot and RT-qPCR for depletion and target validation, RNA-seq for global transcript analysis, apoptosis and proliferation assays to measure functional outcomes, and co-immunoprecipitation/RNA immunoprecipitation for interaction studies. Reporter assays for p53 and MYC activity, together with migration and invasion tests, further enable detailed phenotypic characterization. This polyclonal population is suitable for functional genomics screens, drug sensitivity profiling, and mechanistic studies of RNA-based regulation in colorectal cancer. For additional information or custom requests, contact Ascent Research.
