The HNRNPLL Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, engineered to disrupt the HNRNPLL gene. This polyclonal pool provides a loss-of-function model for investigating the role of HNRNPLL-mediated alternative splicing in cancer biology.
HT29 cells, originally established from a primary tumor of a 44-year-old female with colorectal adenocarcinoma, serve as a well-characterized intestinal epithelial model. These adherent cells are widely employed in studies of colorectal cancer, differentiation, and signaling pathways such as Wnt and epithelial-mesenchymal transition (EMT).
HNRNPLL encodes an RNA-binding protein that regulates alternative splicing of key pre-mRNAs, including CD45 (PTPRC), CD44, FGFR2, CTNND1, and CDH1. Its activity is modulated by upstream regulators TGF-beta, Wnt3a, and the MYC transcription factor. HNRNPLL interacts with core spliceosome components such as U1 and U2 snRNPs and splicing factors SRSF1, U2AF2, and PTBP1. Through these interactions, HNRNPLL controls the alternative splicing of targets that influence downstream signaling: CD45 splicing impacts LCK and FYN in immune cells; alternative splicing of CD44 and CDH1 modulates beta-catenin and TCF/LEF within the Wnt pathway, thereby regulating epithelial-mesenchymal transition and cell adhesion. In HT29 cells, HNRNPLL knockout disrupts these splicing networks, providing a model to study how aberrant splicing contributes to colorectal cancer progression.
In the HT29 colorectal cancer context, disruption of HNRNPLL alters the splicing patterns of genes central to EMT and Wnt signaling. This knockout model enables dissection of how HNRNPLL-dependent splicing changes modulate cell adhesion, invasion, and tumor progression. The polyclonal format avoids clonal selection bias and provides a robust population for functional studies.
This product is suited for a range of research applications, including alternative splicing analysis via RNA-seq and RT-qPCR for specific splice variants, EMT functional assays such as wound healing and transwell invasion, and drug target validation. It also supports immunofluorescence for E-cadherin localization, western blotting for downstream targets, and flow cytometry for CD44 expression. These assays facilitate mechanistic studies in colorectal cancer, inflammatory bowel disease, and autoimmune disorders. For further details or assistance with experimental design, please contact Ascent Research.
