The CASP7 Knockout 786-O Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of 786-O cells with targeted disruption of the CASP7 gene. This heterogeneous pool maintains genetic diversity and is ideal for bulk loss-of-function studies without single-cell cloning. The CRISPR approach introduces gene disruption across the population, enabling robust interrogation of caspase-7-related phenotypes.
The 786-O host cell line is a well-characterized human clear cell renal cell carcinoma (ccRCC) line derived from the primary renal cell adenocarcinoma of a 58-year-old male. These cells harbor a mutant VHL tumor suppressor gene, a hallmark of ccRCC, and display typical epithelial morphology with tumorigenic properties. The 786-O line is widely used as an in vitro model for renal cancer research, particularly for exploring VHL-mediated signaling, hypoxia response pathways, and mechanisms of oncogenic transformation in kidney epithelial cells.
CASP7 encodes caspase-7, an executioner caspase activated by initiator caspases-8 and -9 downstream of extrinsic and intrinsic apoptotic signals, respectively. Activated caspase-7 cleaves multiple substrates including PARP, lamin A/C, and DFF45, driving DNA fragmentation and nuclear disassembly. Its activity is inhibited by XIAP, c-IAP1, and c-IAP2, with release by SMAC/DIABLO. In the intrinsic pathway, cytochrome c and Apaf-1 activate caspase-9, regulated by BAX, BAK, Bcl-2, Bcl-xL, and BID. Extrinsic activation involves death receptor ligands TRAIL and FasL. Caspase-7 also integrates DNA damage responses through p53 signaling, positioning it at a convergence point of multiple apoptotic stimuli.
In the context of ccRCC, apoptosis resistance is a critical factor in tumor progression and therapeutic failure. The 786-O cell line, with its VHL mutation, provides a unique platform to study the interplay between hypoxia-inducible factor (HIF) regulation and apoptotic signaling. Disruption of CASP7 in this background allows researchers to dissect caspase-7??s contribution to cell death pathways that may be dysregulated in renal cancer. This polyclonal knockout model is particularly useful for assessing how the loss of caspase-7 function impacts sensitivity to standard chemotherapeutics or targeted agents, and for identifying compensatory survival mechanisms that emerge in the absence of this executioner caspase.
Typical applications include apoptosis mechanistic studies, pro-apoptotic compound screening, and drug resistance research in renal carcinoma. Researchers can employ Western blotting, RT-qPCR, and Sanger sequencing for confirmation, along with functional assays such as caspase-3/7 activity, PARP cleavage, Annexin V flow cytometry, and MTT viability testing. This product supports detailed caspase-7 pathway analysis and therapeutic profiling. For further details, contact Ascent Research.
