The HCFC1R1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human ovarian adenocarcinoma cell line SK-OV-3, featuring targeted disruption of the HCFC1R1 (PBXIP1) gene. This product provides a heterogeneous knockout model suitable for studying loss-of-function effects in a relevant cancer background without clonal selection, ensuring representation of diverse editing events across the cell pool.
The parental SK-OV-3 cell line is an ascites-derived epithelial ovarian adenocarcinoma model with a TP53-null genetic background and inherent resistance to platinum-based chemotherapies. This cell line is widely used to investigate aggressive ovarian cancer phenotypes, drug resistance mechanisms, and metastasis, making it a clinically relevant host for gene knockout studies.
HCFC1R1 encodes a scaffold protein that integrates signals from multiple oncogenic pathways. It is activated downstream of estrogen signaling and growth factors such as EGF and IGF-1, and interacts with PBX1, estrogen receptor alpha, and HCFC1 to enhance PI3K/AKT and MAPK/ERK cascade activity. Through these interactions, HCFC1R1 promotes phosphorylation of AKT and ERK1/2, leading to increased cyclin D1 expression and cell cycle progression. Additionally, HCFC1R1 stabilizes ??-catenin by modulating GSK-3?? activity, thereby potentiating TCF/LEF-mediated transcription and Wnt target gene expression. This scaffold also drives epithelial-mesenchymal transition by transcriptionally upregulating Snail and MMP9, facilitating tumor cell invasion and metastasis.
Disruption of HCFC1R1 in the SK-OV-3 background offers a powerful tool to dissect the scaffold??s contributions to ovarian cancer aggressiveness, particularly in the context of TP53 deficiency and platinum resistance. Because HCFC1R1 simultaneously engages PI3K/AKT, MAPK, and Wnt/??-catenin signaling nodes, loss of its expression is expected to attenuate proliferative, migratory, and invasive capacities that are typically exacerbated in this refractory disease model. Researchers can therefore employ this polyclonal knockout population to interrogate how HCFC1R1 sustains the malignant phenotype and whether its ablation restores sensitivity to DNA-damaging agents or PARP inhibitors.
Typical research applications include examining the impact of HCFC1R1 loss on SK-OV-3 cell proliferation by MTT assay, migration and invasion using Transwell chambers, and EMT marker expression via western blotting and RT-qPCR. The polyclonal knockout cells are also suited for drug sensitivity profiling with platinum compounds or PARP inhibitors, immunofluorescence localization of ??-catenin or Snail, and in vivo tumor growth assessments in xenograft models. Flow cytometry can further be utilized to evaluate cell cycle distribution and apoptosis upon pathway perturbation. For further technical inquiries, please contact Ascent Research.
