The BICC1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with disrupted BICC1 gene expression. This heterogeneous loss-of-function model, based on the SK-HEP-1 hepatic adenocarcinoma cell line, enables investigation of BICC1-dependent post-transcriptional regulation without clonal selection artifacts.
Derived from ascites of a liver adenocarcinoma patient, SK-HEP-1 cells represent a neoplastic epithelial background with endogenous Wnt and TGF-?? pathway components. This hepatic adenocarcinoma model is widely used to study hepatocellular carcinoma cell biology, including proliferation, migration, and drug resistance. Its relevance extends to BICC1-associated pathologies such as polycystic kidney disease, given shared signaling axes.
BICC1 encodes an RNA-binding protein that represses translation by binding 3??UTRs and recruiting the CCR4-NOT deadenylase complex. A key target is Dishevelled (DVL1/2) mRNA; BICC1-mediated silencing attenuates Wnt/??-catenin signaling downstream of WNT, FZD, and the AXIN?CGSK3?? destruction complex. Knockout therefore elevates DVL, stabilizes ??-catenin, and upregulates TCF/LEF targets like MYC and CCND1. BICC1 also interacts with SMAD1/5 to influence TGF-?? signaling and modulates PTH mRNA stability. Upstream regulation by Wnt ligands, TGF-?? ligands, and PKC positions BICC1 as a critical node linking Wnt, TGF-??, and planar cell polarity pathways.
In SK-HEP-1 cells, BICC1 disruption allows dissection of post-transcriptional control over Wnt-driven phenotypes, including ??-catenin-dependent proliferation and invasion. This model can reveal how BICC1 loss enhances oncogenic signaling in a liver cancer background, and it permits exploration of cell polarity defects and cross-talk with TGF-??/SMAD signaling. The polyclonal nature preserves population-level heterogeneity, which is advantageous for studying drug sensitivity and resistance mechanisms.
Applications include RT-qPCR, RNA-seq, Western blotting, and TOP/FOP flash reporter assays to verify pathway activation. Co-immunoprecipitation confirms BICC1?CDVL interactions, while phenotypic assays (MTT/CCK-8, transwell migration, flow cytometry) characterize proliferation, migration, and apoptosis. Drug screening with agents such as ICG-001 or XAV939 can identify BICC1-dependent therapeutic vulnerabilities. For further inquiries, contact Ascent Research.
