The HNRNPDL Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HNRNPDL gene in the human SK-HEP-1 liver adenocarcinoma cell line. This model employs a heterogeneous population of cells with disrupted HNRNPDL alleles, generated through CRISPR/Cas9-mediated gene disruption, enabling loss-of-function studies. The polyclonal nature retains biological variability while providing a robust system for investigating HNRNPDL-dependent post-transcriptional regulation. The knockout cells serve as a valuable tool for examining the functional consequences of HNRNPDL ablation in a tumorigenic epithelial background.
The parental SK-HEP-1 cell line is a widely used human hepatocellular carcinoma model derived from the ascites fluid of a patient with liver adenocarcinoma. These epithelial cells exhibit characteristics of advanced liver cancer and are employed in studies of tumor biology, metastasis, and therapeutic response. The SK-HEP-1 background provides a clinically relevant context for dissecting molecular pathways involved in hepatocarcinogenesis and for evaluating potential anticancer interventions.
HNRNPDL encodes an RNA-binding protein that functions as a key regulator of alternative splicing, mRNA stability, and intracellular transport. It interacts with spliceosome components such as SRSF1, U2AF1, and SF3B1, and cooperates with other hnRNP family members, including HNRNPA1 and HNRNPA2B1. The protein is regulated by upstream signaling from MAPK and AKT kinases, as well as the DNA damage response pathway. Downstream, HNRNPDL controls the alternative splicing of BCL2L1 and modulates the expression of cell cycle regulators such as CCND1, thereby influencing proliferation and apoptosis.
In the SK-HEP-1 adenocarcinoma model, disruption of HNRNPDL is expected to impair post-transcriptional control of mRNAs critical for tumor cell survival and growth. Loss of HNRNPDL function alters the splicing patterns of BCL2L1, shifting the balance between pro- and anti-apoptotic isoforms, and reduces CCND1 expression, potentially attenuating cell cycle progression. The resulting phenotype may include diminished tumorigenic properties, making this knockout population a powerful system for investigating the contribution of RNA processing to liver cancer malignancy.
These polyclonal knockout cells are suited for a range of experimental applications, including analysis of alternative splicing mechanisms by RT-PCR splicing assays or RNA-seq, protein interaction studies via co-immunoprecipitation, and functional profiling through cell viability, apoptosis, and migration assays. They facilitate the characterization of HNRNPDL-dependent post-transcriptional networks and support drug target discovery efforts in liver cancer. For additional information, please contact Ascent Research.
