The HCFC1R1 Knockout 786-O Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HCFC1R1 gene in human 786-O renal cell carcinoma cells. This heterogeneous pool of edited cells provides a loss-of-function model that avoids clonal selection bias, enabling studies in a genetically diverse cellular context. The CRISPR/Cas9-mediated disruption aims to suppress HCFC1R1 expression, facilitating the investigation of gene function without introducing specific sequence alterations. This product is designed for advanced applications in cancer biology and transcriptional regulation.
The parental 786-O cell line is an adherent epithelial model derived from a human renal cell carcinoma, characterized by a mutation in the VHL tumor suppressor gene. This mutation results in constitutive HIF pathway activation and serves as a widely utilized system for renal cell carcinoma research. The adherent growth property supports diverse culture and assay formats. The VHL-null background underpins studies of tumor metabolism, angiogenesis, and drug susceptibility.
HCFC1R1 encodes a protein that regulates the transcriptional coactivator HCF-1, a critical factor for E2F-dependent cell cycle progression and chromatin remodeling. HCFC1R1 interacts with HCF-1, the glycosyltransferase OGT, and transcription factors E2F1 and Oct-1, modulating the expression of downstream targets such as cyclin D1 and stress-responsive genes. This regulatory network is activated by E2F transcription factors and cell cycle kinases, linking mitogenic signals to gene expression. Knockout of HCFC1R1 disrupts HCF-1 complex formation, potentially impairing coordinated cell cycle entry and altering chromatin states.
In the 786-O renal carcinoma model, the absence of HCFC1R1 allows dissection of HCF-1-mediated pathways against a VHL-mutant background. The knockout enables exploration of how HCFC1R1 influences proliferation, differentiation, and stress responses in kidney cancer cells. This system is particularly valuable for investigating the interplay between hypoxia signaling, cell cycle control, and chromatin dynamics, and for examining the role of HCF-1 complexes in viral infection susceptibility. Such studies contribute to understanding renal cell carcinoma pathogenesis and the molecular consequences of HCFC1R1 loss.
This polyclonal knockout cell population is suitable for renal cell carcinoma biology research, cell cycle studies, transcriptional regulation analysis, and host-virus interaction investigations. Assays such as Western blotting, RT-qPCR, RNA-seq, ChIP-seq, proliferation and colony formation assays, viral infection assays, immunofluorescence, and flow cytometry are readily applicable. The polyclonal format captures heterogeneous knockout effects, providing a more physiologically relevant model than clonal derivatives. For further details, please reach out to Ascent Research.
