The BRSK2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human hepatic adenocarcinoma cell line SK-HEP-1, designed for loss-of-function studies of the serine/threonine kinase BRSK2. This product contains a heterogeneous pool of cells with targeted disruption of the BRSK2 gene, avoiding clonal selection and preserving natural population variability. The use of CRISPR/Cas9-mediated gene disruption enables robust investigation of BRSK2-dependent effects in a widely used liver cancer model.
The parental SK-HEP-1 cell line was originally established from the ascitic fluid of a male patient with liver adenocarcinoma and exhibits both hepatic and endothelial characteristics. These cells display morphological and molecular features of vascular endothelial cells, including the expression of certain adhesion molecules and angiogenic factors, making them a unique in vitro system for studying tumor?Cendothelial interactions, hepatic sinusoidal biology, and the tumor microenvironment in liver cancer.
BRSK2 is a member of the AMPK-related kinase family that functions downstream of the tumor suppressor LKB1 (STK11) and its cofactors MO25 and STRAD. Upon LKB1-mediated phosphorylation, BRSK2 phosphorylates key substrates such as the microtubule-associated protein Tau (MAPT), the cell cycle regulators Wee1 and CDC25, and the mTORC1 component Raptor. These interactions place BRSK2 at the intersection of neuronal polarization, cell cycle progression, and metabolic signaling, with additional roles in insulin secretion potentially mediated through ??-tubulin modulation.
In the SK-HEP-1 background, disruption of BRSK2 provides a relevant model to dissect its function in liver cancer cell biology. The endothelial-like features of the host cells allow exploration of BRSK2’s impact on tumor cell proliferation, migration, and metabolic adaptation, while the polyclonal nature of the knockout mirrors the genetic heterogeneity often observed in tumors. This system is particularly suited to study the LKB1?CBRSK2 axis and its influence on cell cycle checkpoints through Wee1/CDC25 and on cytoskeletal dynamics via Tau phosphorylation.
Researchers can employ this knockout model across a variety of functional assays, including Western blotting, RT-qPCR, cell proliferation and wound healing assays, transwell invasion assays, flow cytometry-based cell cycle analysis, and in vitro kinase activity measurements. These applications enable detailed investigation of BRSK2 in cancer cell signaling, metabolic disease modeling, and neurobiology, especially within the context of hepatic adenocarcinoma and endothelial biology. For detailed product information and custom inquiries, please contact Ascent Research.
