The GTF2IRD1 Knockout SK-HEP-1 Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population engineered from the SK-HEP-1 human liver adenocarcinoma cell line. These cells carry targeted disruption of the GTF2IRD1 gene, generating a loss-of-function model suitable for studying the transcriptional regulatory roles of this factor. The polyclonal nature of the population preserves functional heterogeneity while providing a robust tool for functional genomics and phenotypic screening, eliminating the need for extensive single-cell clonal validation.
SK-HEP-1 is a liver adenocarcinoma cell line established from a 52-year-old male, widely utilized to study hepatic tumorigenesis and metastatic progression. As an adherent line with endothelial-like characteristics, it facilitates investigations of adhesion, migration, and drug resistance in liver cancer. This cellular background is inherently tumorigenic, providing a relevant platform for examining how GTF2IRD1 knockout impacts cancer-relevant phenotypes such as proliferation and invasive capacity.
GTF2IRD1 is a transcription factor of the TFII-I family that governs craniofacial morphogenesis and neural crest specification by regulating developmental gene expression. It interacts with TFII-I, HDAC1/2, and SWI/SNF components to modulate transcription of HOX and DLX family genes. Located within the Williams-Beuren syndrome critical region, GTF2IRD1 disruption is linked to craniofacial and neurodevelopmental abnormalities. In cancer, its context-dependent roles in proliferation and adhesion highlight its potential as a tumor-related factor.
CRISPR/Cas9 knockout of GTF2IRD1 in SK-HEP-1 cells is expected to disrupt transcriptional networks governing adhesion, migration, and proliferation, key processes in hepatic tumorigenesis. This model enables dissection of GTF2IRD1-dependent pathways in a cancer context, potentially revealing tumor-suppressive or oncogenic functions. The polyclonal population allows assessment of phenotypic variability across a heterogeneous pool, mirroring tumor heterogeneity. Researchers can investigate how GTF2IRD1 loss alters downstream target expression and drug responses, advancing liver cancer biology and therapeutic research.
This polyclonal knockout product supports functional genomics and cancer biology studies, with assays including RNA-seq, RT-qPCR, and Western blotting to characterize transcriptomic and proteomic changes. ChIP-qPCR can assess GTF2IRD1 promoter occupancy. Migration, invasion, and proliferation assays enable analysis of metastatic potential, while drug sensitivity testing explores chemoresistance. Additionally, it serves as a disease model for Williams-Beuren syndrome, facilitating in vitro investigation of neural crest and craniofacial gene regulation. For further technical inquiries, contact Ascent Research.
