The BRSK2 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the HCT 116 human colorectal carcinoma line, engineered to achieve functional disruption of the BRSK2 gene. This loss-of-function model enables systematic dissection of BRSK2-mediated pathways in a well-characterized colorectal cancer background, providing a reproducible tool for studying tumor biology and therapeutic responses.
HCT 116 is an epithelial cell line isolated from a colorectal carcinoma, carrying activating mutations in KRAS and ???catenin that drive constitutive Wnt signaling and oncogenic growth. This line is widely employed as a model system for colorectal cancer research, including studies of signal transduction, drug sensitivity, and metastatic potential, owing to its stable genotype and amenability to genetic manipulation.
BRSK2 encodes a serine/threonine kinase belonging to the AMPK-related family, activated by LKB1 (STK11)-dependent phosphorylation in a complex with STRAD and MO25. Once activated, BRSK2 phosphorylates key cell cycle regulators WEE1 and CDC25C to control G2/M transition, and targets ???tubulin (TUBG1) to govern centrosome duplication. It also interacts with 14?3?3 proteins and contributes to autophagy and mTOR signaling downstream of energy stress, positioning it at the intersection of metabolic sensing and cell division.
In the context of HCT 116 cells, which harbor a hyperactive KRAS?Wnt axis, loss of BRSK2 is particularly informative for evaluating its tumor?suppressive functions, as BRSK2 is a substrate of the tumor suppressor kinase LKB1. Disruption of BRSK2 allows researchers to assess alterations in cell cycle progression, centrosome homeostasis, and sensitivity to chemotherapeutics or targeted agents, and to explore synthetic lethal interactions with the oncogenic background.
Key applications of this polyclonal knockout product include Western blotting to confirm loss of BRSK2 and phospho?substrate levels, flow cytometric analysis of cell cycle distribution, immunostaining for centrosomal markers, proliferation and colony formation assays, and in vivo xenograft tumor growth studies. It is ideally suited for functional genomics, drug target validation, and mechanistic studies in colorectal cancer and related signaling disorders. For additional information or to order, please contact Ascent Research.
