The ALB Knockout 786-O Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the ALB gene in the 786-O human cell line. This heterogeneous pool of edited cells provides a loss-of-function model for studying albumin biology in a renal cell carcinoma context. Unlike single?clone isolates, the polyclonal format preserves background genetic diversity, facilitating experiments that require population-level readouts such as metabolic profiling or drug sensitivity assays. The product is supplied as a live cell stock suitable for immediate expansion in adherent culture, with no additional selection markers engineered.
The parental 786-O line is an adherent epithelial cell model derived from a primary clear cell renal cell carcinoma. These cells harbor a well?characterized VHL deficiency that leads to stabilization of hypoxia?inducible factors, particularly HIF?2??, and recapitulate key features of renal adenocarcinoma. As a mainstay in kidney cancer research, 786-O cells are widely employed to investigate VHL?dependent tumor suppression, hypoxia?driven oncogenic signaling, and metabolic reprogramming. Their human origin and ease of culture make them a versatile platform for probing gene function in a clinically relevant tumor background.
Albumin (ALB) is conventionally recognized as a major plasma protein, but accumulating evidence supports additional intracellular and pericellular roles in uptake of fatty acids, hormones, and xenobiotics. In the cellular environment, albumin interacts with the secreted protein SPARC and binds to cell surface receptors such as gp60 and caveolin?1, thereby facilitating endocytosis and intracellular lipid delivery. These processes converge on the mTOR/AKT pathway, where fatty acid availability serves as a key input for growth and survival signals. ALB expression is transcriptionally regulated by hepatocyte nuclear factors (HNF1, HNF4), glucocorticoid receptor, and inflammatory cytokines including IL?6 and TNF???, linking its levels to nutritional and inflammatory states.
In the context of 786-O renal carcinoma cells, ALB knockout abrogates albumin?mediated carrier functions, leading to diminished fatty acid uptake and impaired downstream metabolic and pro?survival signaling. Loss of the SPARC?Calbumin interaction is expected to reduce gp60?dependent endocytosis, attenuating mTOR/AKT activation and potentially sensitizing cells to nutrient stress or chemotherapeutic agents. This knockout model thereby enables dissection of albumin??s contribution to tumor cell metabolism, drug internalization, and resistance mechanisms outside the hepatic system. Because 786-O cells naturally overexpress HIF?2??, the ALB?null background additionally offers a tool to study interactions between hypoxia?driven pathways and lipid homeostasis.
Researchers can apply the ALB Knockout 786-O Polyclonal Cells to a broad range of functional studies. These include quantifying albumin secretion by ELISA, analyzing fatty acid uptake flux using fluorescently labeled lipids, and performing drug sensitivity assays (MTT or CCK?8) to assess the impact of albumin loss on chemoresistance. Co?immunoprecipitation and immunofluorescence microscopy can probe physical associations between ALB, SPARC, and gp60, while metabolic flux analysis with Seahorse technology reveals shifts in oxidative phosphorylation or glycolysis. The model also supports investigation of albumin?based nanoparticle delivery systems and tumor microenvironment crosstalk. For further details or technical assistance, please contact Ascent Research.
