DNASE1L1 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian carcinoma epithelial cell line. This product contains a heterogeneous pool of cells with targeted disruption of the DNASE1L1 gene, which encodes a secreted endonuclease responsible for extracellular DNA degradation. The polyclonal format ensures a diverse loss-of-function model that eliminates clonal artifacts and provides a robust experimental system for studying the role of DNASE1L1 in ovarian cancer biology.
The MES-OV cell line is an established model of ovarian carcinoma, exhibiting typical epithelial morphology and tumorigenic properties. Originating from a human ovarian adenocarcinoma, these cells are widely utilized in cancer research to investigate tumor progression, metastasis, and drug responses. Their epithelial origin and malignant phenotype make them particularly relevant for dissecting the molecular mechanisms underlying ovarian cancer pathogenesis and identifying potential therapeutic targets.
DNASE1L1 functions as a secreted endonuclease that degrades extracellular DNA during apoptosis and cellular debris clearance. It acts downstream of caspase-3 and is linked to the cytochrome c/APAF-1 apoptosome pathway. Transcriptionally regulated by p53, its expression is also induced by TNF-alpha and IL-6. DNASE1L1 interacts with actin and is influenced by ICAD to modulate chromatin fragmentation. By reducing extracellular DNA levels, it prevents activation of cytosolic DNA sensors such as cGAS-STING and dampens innate immune signaling. Therefore, DNASE1L1 knockout leads to accumulation of immunostimulatory DNA, potentially triggering inflammatory pathways that reshape the tumor microenvironment.
In the context of MES-OV ovarian carcinoma cells, disruption of DNASE1L1 provides a powerful tool to examine how defective DNA degradation influences tumor biology. The polyclonal knockout cells enable investigation of apoptosis resistance, as failure to clear extracellular DNA may promote chronic inflammation and affect cancer cell survival. Additionally, this model allows researchers to explore how accumulated DNA activates the cGAS-STING pathway, potentially modulating the tumor immune landscape and influencing metastasis. The MES-OV background ensures physiologically relevant studies in an epithelial ovarian cancer setting, facilitating translation of findings to clinical research.
This knockout model supports diverse assays such as TUNEL and comet assays for DNA damage, Western blotting for cleaved caspase-3 and PARP, and RT-qPCR for DNASE1L1 expression. Flow cytometry (Annexin V/PI) assesses viability, while Transwell assays measure migration and invasion. ELISA quantifies extracellular DNA. These tools enable drug sensitivity screening, DNA damage response studies, and tumor microenvironment analyses. For ordering information, contact Ascent Research.
