The BACH1 Knockout SK-HEP-1 Polyclonal Cells comprise a heterogeneous population of CRISPR/Cas9-edited SK-HEP-1 cells with disruption of the BACH1 gene. As a polyclonal knockout cell product, this model provides a loss-of-function system that avoids clonal selection artifacts and preserves cellular heterogeneity. The genetic disruption is achieved through standard CRISPR/Cas9 gene editing, yielding a mixed knockout population suitable for comparative functional genomic analyses. This product is designed for advanced research into oxidative stress, cancer biology, and drug resistance mechanisms.
SK-HEP-1 is a human liver adenocarcinoma cell line isolated from ascites fluid. Although of epithelial origin, it displays an endothelial-like phenotype and is widely used as a hepatocellular carcinoma model. These adherent cells exhibit high migratory and invasive capacity, making them particularly valuable for metastasis studies. SK-HEP-1 cells retain functional p53 and active NRF2 signaling pathways, both of which are directly linked to BACH1-mediated transcriptional regulation. This unique background facilitates investigation of epithelial-mesenchymal transition (EMT), tumor angiogenesis, and heme signaling.
BACH1 encodes a transcriptional repressor that competes with NRF2 for binding to antioxidant response elements (AREs), thereby modulating genes such as heme oxygenase-1 (HMOX1) and NAD(P)H dehydrogenase quinone 1 (NQO1). Under basal conditions, BACH1 heterodimerizes with small Maf proteins to repress ARE-driven transcription; elevated heme or oxidative stress triggers its degradation. BACH1 also represses the metastasis suppressor RKIP and epithelial marker E-cadherin, while activating prometastatic CXCR4 and matrix metalloproteinases MMP1 and MMP9. Its activity is regulated by NRF2, heme, hypoxia, and microRNAs including miR-196a and miR-27a, and it interacts with corepressor complexes containing HDAC1 and CoREST. Thus, BACH1 serves as a nexus between oxidative stress adaptation and metastatic progression.
Disruption of BACH1 in SK-HEP-1 cells is anticipated to enhance NRF2-mediated antioxidant gene expression and reduce metastatic traits. This model permits investigation of altered cellular responses to oxidative stress, chemotherapeutics such as sorafenib, or heme-induced cytotoxicity. The inherently invasive SK-HEP-1 background, combined with BACH1??s regulation of critical metastasis regulators like RKIP, E-cadherin, and CXCR4, provides an optimal system for dissecting liver cancer metastasis. Furthermore, the polyclonal nature avoids biases introduced by single-cell cloning, more accurately reflecting tumor heterogeneity.
Representative applications include western blotting and RT-qPCR to confirm BACH1 knockout, RNA-seq for transcriptomic profiling, and ChIP-qPCR to assess BACH1 occupancy at AREs. Functional assays such as migration and invasion tests, immunofluorescence, and flow cytometry enable characterization of metastatic and protein expression changes. Drug sensitivity assays, luciferase reporter measurements of NRF2 activity, and co-immunoprecipitation studies of residual protein interactions are also feasible. For additional information, please contact Ascent Research.
