The HSPA1L Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line, engineered to disrupt HSPA1L function. This heterogeneous pool of cells with targeted gene disruption enables robust loss-of-function studies of HSPA1L-mediated chaperone activities in a cancer model.
SK-HEP-1 is a hepatic adenocarcinoma cell line established from the ascites of a 52-year-old male with liver cancer. It exhibits endothelial-like properties and is implicated in tumor angiogenesis and metastasis, offering a unique model to study liver cancer biology and vascular mimicry.
HSPA1L encodes a stress-inducible member of the HSP70 chaperone family that maintains proteostasis by facilitating protein folding and refolding, and regulates apoptosis via interactions with BCL2 and AKT. Transcriptionally controlled by HSF1, its expression rises under heat shock, oxidative stress, hypoxia, and TNF?? stimulation. HSPA1L cooperates with co-chaperones such as DNAJB1, BAG proteins, CHIP/STUB1, and HOP/STIP1, and influences signaling through HSP90AA1, MAPK8, and HSPH1. Disruption of HSPA1L compromises these networks, leading to accumulation of misfolded proteins, impaired stress response, and altered cell survival signaling through PI3K/AKT and MAPK/ERK pathways.
In the SK-HEP-1 background, loss of HSPA1L is expected to attenuate stress adaptation in the tumor microenvironment, reduce angiogenic potential, and sensitize cells to apoptosis. This knockout model thus aids in dissecting how chaperone-mediated signaling supports hepatocellular carcinoma progression, metastasis, and drug resistance.
This product is suited for investigating heat shock response and chaperone-dependent survival in liver cancer, testing chemotherapeutic sensitivity, and modeling male infertility due to HSPA1L??s role in spermatogenesis. Key assays include Western blotting, RT-qPCR, cell viability, Annexin V apoptosis, migration/invasion, proteasome and chaperone activity measurements, and transcriptomic profiling via RNA-seq. For more information, contact Ascent Research.
