The HMMR 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. This product features disruption of the HMMR gene, which encodes the hyaluronan-mediated motility receptor. The polyclonal format provides a heterogeneous knockout pool, enabling loss-of-function studies without the need for single-cell clone isolation. The knockout cells are useful for investigating HMMR-dependent signaling and cellular behaviors in a liver cancer context.
SK-HEP-1 is a human liver adenocarcinoma epithelial cell line originally isolated from ascitic fluid. This cell line serves as an established model for studying hepatocellular carcinoma biology, including tumor growth, migration, and invasion. The epithelial origin and hepatic identity make SK-HEP-1 cells particularly suitable for examining HMMR-mediated hyaluronan signaling and its role in liver cancer metastasis.
HMMR (hyaluronan-mediated motility receptor, also known as RHAMM) is a cell surface receptor that binds the extracellular matrix glycosaminoglycan hyaluronan (HA). Upon HA binding, HMMR interacts with CD44 to activate multiple downstream signaling cascades, including the ERK1/2 and AKT pathways. Key downstream effectors include the small GTPases Rac1 and RhoA, which coordinate cytoskeletal dynamics and cell motility, while ERK1/2 and AKT promote cell proliferation and survival. Additional interacting factors such as cortactin, tubulin, and the actin cytoskeleton further link HMMR signaling to cell migration machinery. The HMMR-CD44-HA signaling axis regulates expression of matrix metalloproteinases (MMPs), contributing to extracellular matrix remodeling and invasive behavior.
In liver adenocarcinoma, HMMR is often overexpressed and correlates with enhanced metastatic potential and poor prognosis. Disruption of HMMR in SK-HEP-1 cells therefore provides a relevant loss-of-function model to examine hyaluronan-driven signaling pathways involved in liver cancer cell migration, invasion, and proliferation. By eliminating HMMR expression, these knockout cells enable researchers to dissect the contribution of HMMR to CD44-mediated signaling and to evaluate the dependency of liver cancer cells on this receptor for metastatic behavior. This model also facilitates identification of alternative compensatory mechanisms that may be activated upon HMMR loss.
Researchers can employ this knockout population in a wide range of cell-based assays to characterize the functional consequences of HMMR depletion. Western blotting and RT-qPCR can be used to verify HMMR protein and mRNA knockdown, respectively. Transwell migration and invasion assays reveal alterations in chemotactic and invasive capacity, while MTS/MTT assays assess changes in cell proliferation. Hyaluronan binding assays determine the ability of cells to interact with the HA matrix, and co-immunoprecipitation with CD44 demonstrates disruption of receptor complex formation. These applications support drug targeting studies aimed at interfering with hyaluronan-mediated motility in liver cancer. For further technical information or to place an order, please contact Ascent Research.
