The BCL7B Knouckout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the BCL7B gene has been disrupted via CRISPR/Cas9-mediated gene editing in the human SK-HEP-1 cell line. This polyclonal pool consists of a heterogeneous mix of edited cells, enabling robust loss-of-function studies without clonal selection. The knockout model is well-suited for investigating the tumor-suppressive functions of BCL7B, a core component of the SWI/SNF chromatin remodeling complex, in a liver cancer-derived context.
SK-HEP-1 is an adherent epithelial cell line originally derived from the ascites of a patient with hepatic adenocarcinoma, serving as a widely used model for hepatocellular carcinoma and liver cancer research. This cell line retains key features of liver cancer pathology, including aberrant Wnt/??-catenin signaling, which is frequently dysregulated in hepatocarcinogenesis. Its genetic and phenotypic characteristics make it an appropriate host for studying gene functions relevant to hepatic tumorigenesis and for screening potential therapeutic agents targeting liver malignancies.
BCL7B functions as a tumor suppressor subunit of the SWI/SNF chromatin remodeling complex, interacting with core components SMARCA4, SMARCA2, ARID1A, BAF155, BAF170, and ACTB to regulate nucleosome positioning and transcription. It is transcriptionally regulated by TCF/LEF factors downstream of Wnt stimulation, integrating signals from FZD and LRP5/6 through CTNNB1 and TCF7L2. In its native context, BCL7B promotes expression of pro?apoptotic factors such as BAX and cell cycle inhibitors like CDKN1A, while repressing adhesion and cytoskeletal genes. Disruption of BCL7B perturbs the terminal output of the Wnt pathway, altering SWI/SNF?mediated chromatin states and transcriptional programs governing cell survival, proliferation, and migration.
In the SK-HEP-1 hepatic adenocarcinoma model, BCL7B knockout provides a physiologically relevant loss-of-function system to dissect the interplay between BCL7B, the SWI/SNF complex, and oncogenic Wnt signaling. BCL7B is frequently downregulated in hepatocellular carcinoma and its loss cooperates with MYC translocation in B?cell malignancies, allowing investigation of common tumor suppressor inactivation mechanisms. The polyclonal population preserves cellular heterogeneity inherent to tumor biology, making it valuable for studying variable responses to pathway perturbations and synthetic lethal interactions in liver cancer cells.
This knockout cell product is suitable for a wide range of functional assays including western blotting, RT?qPCR, RNA?seq, ChIP?seq, co?immunoprecipitation, flow cytometry, cell viability assays, migration/invasion assays, and xenograft tumor growth studies. Researchers can employ the cells to examine BCL7B?dependent changes in SWI/SNF complex assembly, Wnt pathway activation, apoptotic signaling, and cell adhesion. The model also supports drug screening campaigns to identify compounds that selectively target BCL7B?deficient liver cancer cells. For detailed technical information, validation data, and ordering assistance, please contact Ascent Research.
