The AGGF1 Knockout SK-OV-3 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of SK-OV-3 human ovarian adenocarcinoma cells carrying targeted disruptions in the AGGF1 gene. This loss-of-function model enables investigation of AGGF1-dependent processes without the need for single-cell cloning, preserving polyclonal diversity relevant to heterogeneous tumor biology.
The SK-OV-3 parental line was derived from the ascitic fluid of a 64-year-old patient with ovarian adenocarcinoma and recapitulates key features of high-grade serous ovarian carcinoma, including a hypertriploid karyotype, CA125 expression, and mutant TP53. These cells are tumorigenic in vivo and exhibit intrinsic resistance to platinum-based agents such as cisplatin, making them a standard model for studying metastatic progression and chemoresistance.
AGGF1 is an angiogenic factor transcriptionally induced by TNF-?? and HIF-1?? under inflammatory and hypoxic conditions. It physically interacts with TNFR1 and VEGFR2 to trigger downstream activation of the PI3K-Akt and MAPK/ERK signaling axes. Specifically, AGGF1 promotes phosphorylation of AKT at Ser473 and ERK1/2 at Thr202/Tyr204, leading to mTOR complex 1 activation and transcriptional upregulation of VEGF, MMP-2, and MMP-9. These molecular events collectively drive endothelial cell proliferation, migration, and capillary-like tube formation, thereby fostering tumor-associated angiogenesis.
Within the SK-OV-3 milieu, AGGF1-mediated signaling is implicated in sustaining the malignant phenotype, including enhanced angiogenic capacity, peritoneal dissemination, and reduced sensitivity to chemotherapy. By eliminating AGGF1 in this polyclonal knockout pool, researchers can directly assess the gene??s contribution to SK-OV-3 downstream effectors such as AKT and ERK phosphorylation, and evaluate how its loss modulates pro-angiogenic factor secretion and cellular responses to cisplatin. This model thus provides a clinically relevant platform to disentangle AGGF1-dependent versus -independent mechanisms of chemoresistance and metastasis.
These AGGF1 knockout polyclonal cells are well-suited for a spectrum of experimental applications. Standard validation assays include Western blotting for AGGF1 and phosphorylated signaling intermediates (p-AKT, p-ERK1/2) and RT-qPCR quantification of VEGF, MMP-2, and MMP-9 transcripts. Functional angiogenesis studies can be performed using endothelial tube formation and transwell migration/invasion assays, while chemosensitivity is assessed via MTT or clonogenic survival assays with cisplatin. Additional advanced applications include RNA-seq transcriptome profiling, phospho-proteomic analysis, and co-culture systems to examine paracrine effects on endothelial cells. This product enables mechanistic dissection, biomarker discovery, and screening of anti-angiogenic or chemosensitizing compounds in ovarian cancer. For further technical information, please contact Ascent Research.
