The HABP4 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 liver adenocarcinoma cell line. Through CRISPR/Cas9-mediated gene disruption, this product yields a heterogeneous pool of edited cells with targeted loss-of-function of HABP4. The polyclonal format avoids clonal selection biases, offering robust and reproducible phenotypic analysis. These cells are a critical tool for dissecting intracellular roles of HABP4 in hepatocellular carcinoma biology.
The SK-HEP-1 cell line is an epithelial-like hepatic cancer cell line derived from ascitic fluid of a liver adenocarcinoma patient. It serves as a widely used model for hepatocellular carcinoma and cancer metastasis research due to its malignant properties, including anchorage-independent growth and tumorigenicity in vivo. Its metastatic origin makes it particularly suited for studying invasion and migration. SK-HEP-1 cells express relevant hepatic markers and signaling components, providing a physiologically appropriate context for functional analysis of HABP4 in liver cancer.
HABP4, an intracellular hyaluronan-binding protein, integrates extracellular matrix signals with RNA processing and chromatin remodeling. It directly interacts with hyaluronan and CHD3, a core NuRD complex component, linking these signals to transcriptional regulation. PKC-mediated phosphorylation modulates HABP4’s interactions with hyaluronan and RGG box-containing proteins, affecting alternative splicing. HABP4 also transcriptionally regulates cell cycle genes, with downstream targets including cyclins and pre-mRNA processing factors. Key pathway nodes encompass CD44, RHAMM, PKC isoforms, and the CHD3/NuRD complex. Disruption of HABP4 therefore disrupts hyaluronan-dependent signaling, alternative splicing, and chromatin remodeling events.
In hepatocellular carcinoma, HABP4 knockout in SK-HEP-1 cells models the disruption of intracellular hyaluronan signaling that drives liver adenocarcinoma progression. Loss of HABP4 is predicted to impair tumor cell proliferation, migration, and drug resistance by decoupling extracellular hyaluronan from nuclear gene regulatory programs. This model enables dissection of HABP4-mediated alternative splicing events that generate oncogenic isoforms, and reveals how NuRD complex-dependent chromatin changes influence malignancy. It also permits studies on PKC-dependent phosphorylation effects on HABP4 function and its downstream impact on liver cancer metastasis-associated gene expression.
This polyclonal knockout pool is suited for Western blotting, RT-qPCR, and RNA immunoprecipitation to validate HABP4 disruption and assess target gene expression changes. Co-immunoprecipitation and immunofluorescence facilitate mapping of HABP4 interaction networks and subcellular localization. Cell proliferation assays, phospho-signaling analysis, and drug sensitivity studies evaluate functional consequences on liver cancer cell growth and treatment response. RNA-seq reveals transcriptome-wide effects on alternative splicing and gene regulation. These tools collectively support mechanistic investigations of hyaluronan intracellular signaling, RNA processing, and NuRD complex function in hepatocellular carcinoma. For additional technical details or to request a custom quote, please contact Ascent Research.
