The RAD51C Knockout IOSE-80 Cell Line is a CRISPR/Cas9-edited human knockout cell line featuring targeted disruption of the RAD51C gene. This loss-of-function model is generated in the IOSE-80 immortalized ovarian surface epithelial cell background, providing a stable cellular platform for investigating DNA repair and tumor suppressor mechanisms. The product is supplied as a ready-to-use cell line, with gene ablation introduced by CRISPR/Cas9 technology, and serves as a valuable tool for functional genomics studies.
IOSE-80 cells are a well-characterized, non-tumorigenic, immortalized human ovarian surface epithelial cell line. Ovarian surface epithelial cells form the outermost layer of the ovary and play critical roles in ovulation and wound repair processes. The IOSE-80 line retains key epithelial characteristics and offers a physiologically relevant context for studying ovarian cell biology, including responses to genotoxic stress and DNA damage. Its established use in cancer biology research makes it a suitable host for modeling gene functions relevant to ovarian homeostasis and disease.
RAD51C is a central component of the homologous recombination (HR) repair pathway, essential for maintaining genomic integrity. It functions as a RAD51 paralog, forming complexes with RAD51B, RAD51D, XRCC2, and XRCC3 to facilitate RAD51 filament assembly at DNA double-strand breaks. RAD51C is regulated by upstream kinases ATM and ATR, which are activated by DNA damage, and by checkpoint kinase CHEK1. It interacts directly with BRCA-associated proteins BRCA1, BRCA2, and PALB2, thereby linking DNA damage sensing to repair execution. Disruption of RAD51C impairs HR efficiency, leading to accumulation of unrepaired damage, chromosomal instability, and enhanced sensitivity to DNA-damaging agents and PARP inhibitors.
In the IOSE-80 ovarian surface epithelial model, RAD51C knockout abrogates a critical DNA repair axis, rendering cells highly susceptible to genotoxic stress. This deficiency recapitulates molecular features observed in Fanconi anemia complementation group O and hereditary breast and ovarian cancers, where RAD51C mutations are implicated. The knockout cell line therefore provides a unique isogenic system to dissect RAD51C-dependent repair mechanisms in an ovarian epithelial context, enabling the study of cellular responses to chemotherapeutic agents and the exploration of synthetic lethal interactions with PARP inhibitors and other targeted therapies.
Researchers can employ this cell line for a broad spectrum of applications including functional dissection of HR repair, evaluation of PARP inhibitor sensitivity (e.g., olaparib), and investigation of RAD51C mutation impact on genomic stability. Typical experimental workflows encompass western blotting for RAD51C expression validation, immunofluorescence microscopy to assess RAD51 foci formation following DNA damage, comet assays for quantifying DNA lesions, and HR reporter assays to measure repair proficiency. Additionally, RNA sequencing and cell viability assays under drug treatment provide insights into global transcriptional consequences and chemosensitivity profiles. For further information, please contact Ascent Research.
