HSPA6 Knouckout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human SK-HEP-1 hepatic adenocarcinoma cells, engineered for disruption of the HSPA6 gene. This pooled knockout model preserves genomic heterogeneity, avoiding single-cell cloning artifacts. It is ideal for loss-of-function studies examining the stress-inducible chaperone HSPA6 within a genetically diverse edited cell population, suitable for proteostasis and liver cancer research.
The parental SK-HEP-1 cell line was established from ascites of a liver adenocarcinoma patient and is extensively used as a hepatocellular carcinoma model. These epithelial cells retain critical hepatic functions including metabolism, detoxification, and protein secretion, making them relevant for liver cancer and drug metabolism studies. Their robust and reproducible in vitro growth characteristics support long-term experimental use in stress biology research.
HSPA6 encodes a stress-inducible Hsp70 chaperone, activated by HSF1 under heat shock, oxidative stress, and heavy metals. It facilitates folding of nascent and misfolded proteins, preventing aggregation, and interacts with co-chaperones DNAJB1, HSPBP1, BAG3, STUB1, and HOP to mediate protein quality control and degradation via the ubiquitin-proteasome system. In the heat shock response, HSF1-upregulated HSPA6 collaborates with BAG3 to maintain proteostasis. Knockout of HSPA6 abrogates inducible chaperone activity, impairing protein quality control and increasing sensitivity to proteotoxic stress.
In SK-HEP-1 hepatocellular carcinoma cells, HSPA6 disruption compromises cellular adaptation to proteotoxic stress found in the tumor microenvironment, such as hypoxia and chemotherapy. Loss of this inducible chaperone may exacerbate protein aggregation and disrupt secretory homeostasis, promoting cell death under heat shock. This model allows dissection of stress-inducible chaperone contributions to liver cancer survival and proteostasis-driven malignancy. It also enables exploration of related pathologies including ischemia-reperfusion injury and neurodegeneration.
This product is well-suited for mechanistic investigations of the heat shock response in liver cancer, high-throughput drug screening for HSPA6 modulators, and functional assays measuring cell viability, protein aggregation, and apoptosis under proteotoxic stress. Standard techniques such as Western blotting, RT-qPCR, immunofluorescence, and flow cytometry are readily applicable. The polyclonal knockout format also facilitates pooled genetic screens and examination of heterogeneous stress responses. For further technical support, please contact Ascent Research.
