The HTRA1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout population derived from the SK-OV-3 human ovarian adenocarcinoma cell line, providing a loss-of-function model for the HTRA1 serine protease. The polyclonal format, generated by targeted gene disruption, offers a heterogeneous cell pool that avoids clonal biases and is suited for bulk analyses such as pooled functional screens and proteomic studies. These Homo sapiens cells serve as a ready-to-use tool for investigating HTRA1??s tumor-suppressive mechanisms in ovarian cancer.
SK-OV-3 is an epithelial cell line isolated from the ascites of an ovarian adenocarcinoma patient, characterized by epithelial marker expression and tumorigenicity in nude mice. Widely used in ovarian cancer research, it models key aspects of tumor progression, including signal transduction, metastasis, and chemoresistance. This knockout derivative extends the utility of the SK-OV-3 platform to targeted gene perturbation studies.
HTRA1 acts as a secreted serine protease and tumor suppressor by cleaving TGF-?? ligands (e.g., TGF-??1) and receptor TGFBR2, thereby attenuating SMAD2/3 phosphorylation. It also degrades fibronectin and interacts with PDZ proteins like MAGI1 to regulate adhesion and migration. Upstream regulators include p53 and oxidative stress; downstream effects propagate through cyclin D1, p21, BAX/BCL2, and crosstalk with MAPK/ERK and Wnt pathways. This positions HTRA1 as a central inhibitor of TGF-??-driven oncogenic signaling.
In SK-OV-3 cells, HTRA1 knockout relieves TGF-?? pathway inhibition, resulting in sustained SMAD2/3 activation, elevated cyclin D1, and fibronectin accumulation. This molecular profile drives enhanced proliferation, migration, and invasion while reducing apoptosis, mirroring aggressive ovarian cancer behavior. The polyclonal knockout model thus enables mechanistic dissection of how HTRA1 loss contributes to tumor progression and metastasis in an epithelial ovarian carcinoma context.
These cells support diverse experimental workflows, including western blotting for HTRA1 and phospho-SMAD2/3, RT-qPCR, MTT and Transwell assays, Annexin V apoptosis detection, and co-immunoprecipitation with TGF-?? path components. Applications encompass tumor suppressor functional studies, TGF-?? signaling dissection, drug target validation (e.g., cisplatin sensitivity), and RNA-seq transcriptome profiling. For further details or to discuss your experimental needs, please contact Ascent Research.
