The HOMER1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the HOMER1 gene has been disrupted using CRISPR/Cas9-mediated gene editing. This product offers a genetically heterogeneous loss-of-function model derived from the human SK-HEP-1 cell line, enabling functional studies of HOMER1 in hepatic cellular contexts. The polyclonal population retains the diversity of editing outcomes, providing a robust tool for investigating gene function without the clonal biases inherent in single-cell-derived lines.
The SK-HEP-1 host cell line is a human liver adenocarcinoma line originally isolated from the ascites of a patient with liver adenocarcinoma. It exhibits both epithelial and endothelial characteristics, making it a widely used model for hepatic endothelial cell biology and the study of liver cancer metastasis. This dual phenotype allows researchers to explore processes such as angiogenesis, tumor-endothelial interactions, and transdifferentiation in the hepatic microenvironment.
HOMER1 encodes a postsynaptic scaffold protein that links group I metabotropic glutamate receptors (mGluR1/5) to intracellular calcium channels by bridging mGluR5 to inositol 1,4,5-trisphosphate receptors (IP3Rs) and TRPC1 channels, facilitating calcium mobilization and activation of downstream cascades. The protein is regulated by upstream factors including mGluR1/5 activation, ERK1/2, CREB, SRF, and MEF2, and it interacts directly with IP3R, TRPC1, SHANK, CRMP2, PI3K, and GRM5. HOMER1-dependent signaling modulates the MAPK/ERK pathway and cross-talks with the PI3K/AKT/mTOR axis, ultimately influencing calcium-dependent transcription factors such as NFAT. In hepatic cells, these interactions may govern stellate cell activation and fibrogenic responses.
Within the SK-HEP-1 hepatic adenocarcinoma background, disruption of HOMER1 provides a platform to dissect glutamate signaling pathways implicated in liver cancer progression. Given HOMER1’s role in coordinating calcium signaling and cytoskeletal dynamics, this knockout model is particularly suitable for investigating cell migration, invasion, and malignant transformation. Moreover, because the SK-HEP-1 line expresses endothelial markers, the knockout can be applied to study angiogenesis-related crosstalk between tumor cells and the vascular niche. The model also supports research into hepatic stellate cell activation, a process central to liver fibrosis, where HOMER1’s scaffolding function may be critical for transmitting fibrotic signals.
Polyclonal HOMER1 knockout SK-HEP-1 cells are designed for a range of advanced biomedical applications. Researchers can perform Western blotting to confirm loss of HOMER1 protein and monitor phospho-ERK levels, use RT-qPCR to quantify HOMER1 isoform expression, and conduct co-immunoprecipitation to assess interactions with mGluR5 and IP3R. Functional studies may include calcium imaging to measure receptor-operated calcium fluxes, NFAT luciferase reporter assays for transcriptional readouts, and cell migration/invasion assays to evaluate metastatic potential. Drug sensitivity profiling with mGluR5 antagonists offers a pathway-specific pharmacological context. For further technical details, please contact Ascent Research.
