The BCL9L Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma cell line. Generated through CRISPR/Cas9-mediated disruption of the BCL9L gene, this heterogeneous pool of edited cells collectively ablates functional BCL9L protein expression. By avoiding clonal selection, the polyclonal model better reflects the range of genetic perturbations achievable by CRISPR editing, providing a robust loss-of-function system for dissecting BCL9L biology.
The host cell line, SK-HEP-1, is an epithelial cell line originally established from the ascitic fluid of a hepatic adenocarcinoma patient. It is widely used as an in vitro model for hepatocellular carcinoma (HCC), retaining key characteristics such as anchorage-independent growth and tumorigenic potential. SK-HEP-1 cells are well-characterized for their epithelial morphology and are commonly employed to study HCC biology, drug responses, and signaling pathway alterations, making them particularly relevant for investigating liver cancer pathogenesis.
BCL9L (B-cell CLL/lymphoma 9-like) is a transcriptional coactivator in the canonical Wnt/??-catenin pathway. It interacts with ??-catenin and Pygopus (Pygo1/2) cofactors, bridging the ??-catenin/TCF/LEF complex to transcriptional activation machinery, thereby promoting expression of Wnt target genes such as MYC, CCND1, AXIN2, and LGR5. BCL9L functions downstream of Wnt ligand?CFrizzled/LRP5/6 receptor engagement, Dishevelled activation, and ??-catenin stabilization. CRISPR-mediated disruption of BCL9L impairs ??-catenin/TCF-dependent transcriptional programs, enabling dissection of the coactivator’s specific role in Wnt-driven oncogenic transcription.
In hepatocellular carcinoma, Wnt/??-catenin signaling is frequently dysregulated, often via CTNNB1 (??-catenin) mutations. BCL9L knockout in SK-HEP-1 cells allows assessment of HCC dependency on ??-catenin/TCF coactivation for proliferation, survival, and transformation. The polyclonal nature ensures phenotypes reflect consensus gene disruption effects, reducing clonal artifacts. This model is ideal for studying Wnt pathway addiction heterogeneity and validating downstream therapeutic targets in liver cancer.
This BCL9L knockout polyclonal cell product supports diverse research applications. It is suitable for RNA-seq transcriptional profiling to identify BCL9L-dependent gene signatures, as well as RT-qPCR and Western blotting for confirmation of gene disruption. Functional assays include ??-catenin/TCF reporter assays (TOP/FOP Flash), proliferation, and colony formation studies. The model also enables drug screening for Wnt pathway inhibitors and immunofluorescence analysis of ??-catenin localization. For further details, please contact Ascent Research.
