This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HSPA4L gene in SK-HEP-1 cells. The polyclonal format provides a heterogeneous pool of cells with target-gene disruption, generated via CRISPR/Cas9-mediated gene editing, suitable for loss-of-function investigations without the selection biases of clonal isolation.
SK-HEP-1 is a human liver adenocarcinoma cell line derived from the ascites of a patient with hepatocellular carcinoma. These adherent epithelial cells are a well-established model for HCC, widely used to study metastatic progression, drug sensitivity, and tumor pathophysiology. The line retains characteristics relevant to hepatic malignancy and is commonly applied in both in vitro and in vivo oncology research.
HSPA4L functions as an ATP-dependent molecular chaperone essential for protein folding and refolding during cellular stress. Its expression is driven by the HSF1 transcription factor following heat shock, osmotic imbalance, oxidative stress, or inflammatory cytokine exposure. HSPA4L engages with BAG1, BAG3, HSP40, HOP, and CHIP cofactors to modulate client protein conformation and degradation. This chaperone network intersects with MAPK, AKT, and p53 signaling pathways, thereby linking stress responses to cell cycle regulation and apoptosis.
In SK-HEP-1 cells, knockout of HSPA4L compromises the stress-responsive chaperone system, potentially disrupting proteostasis and altering signaling cascades that govern proliferation and cell death. This model is particularly significant for examining how loss of HSPA4L impacts hepatocellular carcinoma behavior, including adaptation to the tumor microenvironment, resistance to chemotherapeutic agents, and metastatic capability. It offers a platform to dissect the contributions of heat shock proteins to hepatocarcinogenesis.
Applications include Western blotting for HSPA4L and apoptosis markers, RT-qPCR analysis of stress-response genes, and cell viability assays under stress conditions. Migration and invasion assays can evaluate metastatic potential, and co-immunoprecipitation can probe chaperone interactions. Phospho-MAPK and AKT signaling studies further elucidate pathway alterations, while drug sensitivity screens assess therapeutic responses. For further information, please contact Ascent Research.
