The HDHD5 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 786-O renal carcinoma cell line, engineered for targeted disruption of the HDHD5 gene. This loss-of-function model enables functional investigation of HDHD5??s biological roles. The polyclonal format represents a heterogeneous pool of edited cells, allowing efficient screening without clonal isolation. It is ideal for interrogating HDHD5-dependent processes in a renal cancer background.
The parental 786-O cell line was established from a primary clear cell renal cell adenocarcinoma and carries a mutation in the VHL tumor suppressor gene. As a VHL-mutant model, 786-O cells exhibit constitutive HIF signaling activation, leading to altered metabolism, angiogenesis, and tumorigenesis. This genetic context makes it a relevant host for studying genes involved in renal cell carcinoma progression. Introducing HDHD5 knockout into this VHL-deficient background allows dissection of possible interactions between HDHD5 hydrolase activity and dysregulated HIF-metabolic pathways.
HDHD5 encodes a haloacid dehalogenase-like hydrolase, predicted to catalyze phosphate ester dephosphorylation. Its substrates and downstream effectors remain largely uncharacterized, but it is hypothesized to participate in cellular metabolic pathways. As a candidate gene for cat eye syndrome, HDHD5 may also have developmental roles. Current knowledge places HDHD5 among a group of understudied hydrolases that modulate small-molecule metabolism, potentially intersecting with key metabolic checkpoints. In 786-O cells, HDHD5 knockout can perturb metabolite pools, enabling functional studies via metabolomics and transcriptomics.
In 786-O cells, loss of HDHD5 provides an opportunity to evaluate whether it acts as a tumor-promoting or -suppressive factor in renal cell carcinoma, especially under defective VHL signaling. Since clear cell renal carcinoma depends on altered metabolic pathways, HDHD5 may influence processes such as lipid and nucleotide metabolism, redox balance, or bioenergetic adaptation. Comparative analysis of wild-type and HDHD5-knockout 786-O cells can reveal changes in proliferation, migration, and invasion, linking HDHD5 function to renal cancer phenotypes.
This polyclonal knockout supports diverse applications, including Western blotting and RT-qPCR for validation, proliferation and migration assays for phenotypic screening, and metabolomics or RNA-seq for systems-level profiling. It is suitable for drug target validation and cancer metabolism research focused on hydrolase-mediated metabolic dysregulation. For additional information or custom requests, please contact Ascent Research.
