BAD Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O renal adenocarcinoma line. This heterogeneous pool contains cells with CRISPR/Cas9-mediated disruptions in the endogenous BAD gene, offering a loss-of-function model for the pro-apoptotic BCL-2 family member BAD. The polyclonal format retains population diversity, useful for studying heterogeneous cancer cell responses.
The parental 786-O line (ATCC CRL-1932) is a clear cell renal cell carcinoma (ccRCC) model originating from a primary renal adenocarcinoma. These tumorigenic epithelial cells retain hallmark features of ccRCC, including aberrant PI3K/AKT/mTOR signaling and HIF pathway activation due to VHL deficiency. Widely used in renal cancer research, the 786-O background provides a clinically relevant setting for apoptosis and drug-resistance studies.
BAD promotes intrinsic apoptosis by binding and neutralizing anti-apoptotic BCL-2 and BCL-xL, enabling BAX/BAK-mediated mitochondrial outer membrane permeabilization and cytochrome c release. Its pro-apoptotic activity is inhibited by phosphorylation via AKT, PKA, RSK, and p70S6K, which triggers 14-3-3 binding and cytoplasmic sequestration. Thus, BAD functions as a critical gateway where survival signaling converges to suppress mitochondrial apoptosis.
In the 786-O ccRCC context, where survival kinases are frequently hyperactivated, BAD knockout removes a pro-apoptotic checkpoint, potentially deepening apoptosis resistance. This model allows researchers to dissect BAD??s specific contribution to apoptosis evasion and chemoresistance in renal cancer, independent of other BCL-2 proteins. It is a valuable tool for examining the interplay between oncogenic signaling and mitochondrial death pathways.
Applications include investigating apoptosis signaling in ccRCC, assessing BAD phosphorylation status by western blot, and performing functional assays such as cytochrome c release, caspase activation, and Annexin V flow cytometry. The model is also suitable for studying BAD??s role in glucose metabolism via glucokinase interaction, and for screening compounds that restore mitochondrial apoptosis. For technical inquiries, contact Ascent Research.
