The BIN1 Knockout SK-HEP-1 Polyclonal Cells product delivers a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the BIN1 gene in the human SK-HEP-1 hepatic adenocarcinoma cell line. This loss-of-function model is generated by CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells that lack functional BIN1 protein. The polyclonal format avoids the clonal selection biases inherent in monoclonal lines, preserving the native cellular heterogeneity critical for robust functional assays and for modeling tumor cell populations. This tool is designed for advanced research applications investigating BIN1-dependent mechanisms in hepatocellular carcinoma and other disease contexts.
The host SK-HEP-1 cell line is a liver adenocarcinoma-derived line originally established from the ascites of a 52-year-old male patient. It serves as a well-characterized in vitro model of hepatocellular carcinoma (HCC) and is widely employed in hepatic drug metabolism studies. SK-HEP-1 cells exhibit many features of liver cancer cells, including dysregulated proliferation and altered metabolic activity, making them a relevant system for dissecting the molecular pathways underlying HCC pathogenesis and for evaluating therapeutic responses in a liver-specific background.
BIN1 functions as a tumor suppressor and adaptor protein in clathrin-mediated endocytosis, with a central role in inhibiting c-MYC transcriptional activity. Mechanistically, BIN1 binds c-MYC and prevents its heterodimerization with MAX, repressing transcription of proliferative targets such as cyclin D1. BIN1 is regulated by upstream signals including c-MYC, E2F1, p53, and EGF receptor signaling. It interacts with dynamin-2, amphiphysin, clathrin, and the ARP2/3 complex, linking the actin cytoskeleton to membrane remodeling during endocytosis. Through these interactions, BIN1 coordinates membrane dynamics and promotes apoptosis via downregulation of BCL2. The knockout model disables both the endocytic scaffolding and the c-MYC-inhibitory functions, enabling systematic dissection of these dual roles.
In hepatocellular carcinoma, BIN1 is frequently downregulated, and its loss enhances c-MYC-driven proliferation. The SK-HEP-1 knockout cells provide a system to investigate how BIN1 ablation affects c-MYC activity, endocytosis, apoptosis, and drug sensitivity. The model also informs studies of actin dynamics and cell migration, processes relevant to metastatic HCC. These cells may additionally support research into breast and prostate cancers and myopathies.
This polyclonal knockout cell population supports Western blotting, RT-qPCR, and co-immunoprecipitation for molecular characterization, transferrin uptake assays for clathrin-mediated endocytosis, flow cytometry for apoptosis, and Transwell migration/invasion assays for metastatic potential. Proliferation and phospho-signaling profiling enable comprehensive pathway analysis. The cells are suitable for rescue experiments. For technical support, please contact Ascent Research.
