The BSDC1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for functional studies of BSDC1 in a human liver adenocarcinoma background. This product comprises a heterogeneous pool of SK-HEP-1 cells with BSDC1 disrupted by CRISPR/Cas9, creating a loss-of-function model. The polyclonal format includes diverse editing events, making it ideal for population-based assays without clonal bias. It serves as an important tool for investigating BSDC1’s role in liver cancer.
SK-HEP-1 is a well-established human liver adenocarcinoma cell line originally derived from the ascites of a patient with hepatocellular carcinoma. This adherent cell line is widely used as a model system for studying liver cancer pathogenesis, drug response, and metastatic behavior. The hepatic origin and malignant phenotype of SK-HEP-1 cells make them particularly relevant for dissecting molecular mechanisms underlying hepatocellular carcinoma. The knockout of BSDC1 in this cell line provides a pertinent platform to explore liver cancer-related transcriptional dysregulation and phenotype alterations.
BSDC1 is a predicted transcriptional regulator containing a BSD domain, a motif found in proteins that modulate gene expression by interacting with the core transcriptional machinery. Mechanistically, BSDC1 is thought to function by engaging key components of the RNA polymerase II transcription system, including potential interactions with TFIIA subunits and chromatin remodeling complexes. Although its upstream activators remain unknown, BSDC1 may lie downstream of oncogenic growth factor signaling pathways active in liver cancer. Putative downstream targets of BSDC1 include genes controlling cell proliferation and differentiation, suggesting that BSDC1 acts as a node in transcriptional networks that sustain malignant growth.
Disruption of BSDC1 in SK-HEP-1 cells is expected to perturb transcriptional programs that drive liver adenocarcinoma phenotypes. This polyclonal knockout model enables researchers to investigate how loss of BSDC1 function alters gene expression signatures associated with cell cycle progression, apoptosis, and invasive potential. By comparing wild-type and knockout populations, scientists can identify BSDC1-dependent regulatory modules that contribute to hepatocellular carcinoma pathology. The model is particularly suited for exploring transcriptional dependencies in liver cancer and for screening potential downstream effectors of BSDC1-mediated regulation.
This knockout model is suitable for functional genomics and liver cancer research. Transcriptomic profiling by RNA-seq, quantitative RT-qPCR, and western blotting enable analysis of gene expression and protein changes. Functional assays such as proliferation, migration, and invasion assays assess phenotypic alterations. These cells provide a robust platform for dissecting BSDC1’s contribution to transcriptional regulation and liver cancer hallmarks. For further information or custom inquiries, please contact Ascent Research.
