This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human clear cell renal cell carcinoma cell line, designed to ablate expression of the DTNB gene. The polyclonal pool provides a heterogeneous population of DTNB-deficient cells, reflecting diverse editing events across the cell population, which is suitable for studying overall gene function without clonal bias. This loss-of-function model enables investigation of DTNB-dependent cellular processes in a relevant cancer cell background.
The 786-O cell line is a widely used model for human clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer. Derived from a primary ccRCC tumor, these cells retain key characteristics of renal carcinoma, including anchorage-independent growth and tumorigenicity in vivo. As an adherent epithelial cell line, 786-O provides a physiologically relevant platform for exploring oncogenic signaling, cell adhesion, and cytoskeletal dynamics in the context of renal malignancy.
DTNB encodes beta-dystrobrevin, a cytoplasmic scaffold protein of the dystrophin-glycoprotein complex (DGC) that links the actin cytoskeleton to the extracellular matrix. It recruits syntrophins (SNTA1, SNTB1) and nNOS (NOS1) to the DGC and is transcriptionally regulated by MYOD1, MEF2C, and SRF. Beta-dystrobrevin interacts with dystrophin (DMD) and utrophin (UTRN), modulating downstream signaling through MAPK1 and AKT1 to control cell adhesion and signal transduction. This scaffold anchors signaling complexes at the membrane, connecting extracellular matrix cues to intracellular pathways such as MAPK/ERK and PI3K/AKT, which are critical for adhesion-dependent survival and migration.
In the context of 786-O renal carcinoma cells, disruption of DTNB expression provides a powerful tool to dissect the role of the DGC in cancer biology. Loss of beta-dystrobrevin may impair DGC-mediated adhesion and signaling, potentially altering cell motility, invasiveness, and proliferation. This model allows researchers to investigate how cytoskeletal scaffolding and extracellular matrix interactions contribute to the malignant phenotype of ccRCC, and to evaluate DTNB as a therapeutic target in renal cell carcinoma or related pathologies such as muscular dystrophy and dilated cardiomyopathy.
This knockout model is suited for a range of functional studies, including Western blotting and immunofluorescence to monitor DGC composition, cell adhesion and scratch wound assays to quantify adhesion and motility, transwell invasion and MTT viability assays to assess invasiveness and proliferation, as well as co-immunoprecipitation and RNA-seq for interaction and transcriptome analyses. These cells further enable drug target validation for muscular dystrophy and cancer. For further information, please contact Ascent Research.
