The BASP1 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in the SK-HEP-1 human hepatic adenocarcinoma cell line, designed as a loss-of-function model for the BASP1 gene. This polyclonal population, generated through CRISPR/Cas9-mediated gene disruption, allows researchers to study BASP1 function in a cellular context with both hepatocyte and endothelial characteristics. The knockout model is suitable for functional assays including proliferation, migration, apoptosis, and transcriptomic analyses, offering a versatile reagent for investigating BASP1-dependent signaling networks without clonal selection.
The SK-HEP-1 cell line was established from ascitic fluid of a 52-year-old male with liver adenocarcinoma. It displays a hybrid phenotype, expressing both hepatocyte and endothelial markers, making it a unique model for hepatocellular carcinoma and endothelial biology. SK-HEP-1 is widely used to investigate molecular mechanisms of liver cancer progression, tumor microenvironment interactions, and endothelial transdifferentiation, providing a distinctive platform for examining how BASP1 influences both epithelial and mesenchymal characteristics.
BASP1 (brain acid soluble protein 1) is a PKC substrate that modulates actin dynamics and calcium/calmodulin-dependent signaling. As a transcriptional co-suppressor for WT1, BASP1 regulates cell proliferation, differentiation, and apoptosis. Phosphorylated by PKC and ERK1/2, it integrates MAPK/ERK pathway signals and cross-talks with PI3K/Akt and Wnt/beta-catenin signaling. Its interacting partners include calmodulin, actin, PRMT1, and WT1, and it influences downstream targets such as c-Myc and cell cycle regulators. Through these interactions, BASP1 controls gene expression programs critical for neuronal development and oncogenesis.
Knockout of BASP1 in SK-HEP-1 cells provides a valuable tool for dissecting oncogenic signaling in hepatocellular carcinoma. Loss of BASP1 perturbs PKC-mediated phosphorylation, alters WT1-dependent transcriptional repression, and impacts the proliferation-apoptosis balance. The endothelial features of SK-HEP-1 also enable exploration of BASP1??s role in endothelial-like transdifferentiation and vascular mimicry, processes linked to aggressive tumor phenotypes. This model facilitates investigation of how BASP1 contributes to cancer cell plasticity within the hepatic microenvironment.
Applications include western blotting and RT-qPCR to verify BASP1 loss and assess downstream targets, immunofluorescence for localization studies, and co-immunoprecipitation for interaction analysis. Migration, invasion, apoptosis, and cell cycle assays can evaluate functional consequences, while RNA-seq reveals transcriptomic changes. This polyclonal knockout product serves as a robust tool for studying PKC signaling, WT1 co-repression, and cancer cell biology. For additional information, please contact Ascent Research.
