The DNAAF2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the DNAAF2 gene in the A2780 human ovarian carcinoma epithelial cell line. This heterogeneous pool of edited cells provides a loss-of-function model without the need for clonal isolation, enabling robust functional studies of DNAAF2. The cells are supplied as a living culture and are suitable for a variety of downstream applications requiring DNAAF2 disruption.
The A2780 cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and is characterized by wild-type p53 status and platinum sensitivity. These adherent epithelial cells serve as a well-established model for ovarian cancer research, particularly for investigating platinum-based chemotherapy responses and resistance mechanisms. Their well-documented genetic background and drug sensitivity profile provide a reliable platform for examining the interplay between ciliary gene function and cancer biology.
DNAAF2 (dynein axonemal assembly factor 2) is a cytoplasmic protein essential for the pre-assembly of inner and outer dynein arm complexes before their transport into cilia. It cooperates with assembly factors DNAAF1 and DNAAF3 and the chaperone HSP90 to facilitate maturation of dynein heavy chains (DNAH5, DNAH11) and associated subunits. Transcriptionally, DNAAF2 is regulated by the master ciliogenic transcription factor FOXJ1 and RFX2, which act downstream of Notch signaling. Disruption of DNAAF2 prevents proper dynein arm formation, leading to loss of ciliary motility and reduced beat frequency.
In the A2780 ovarian cancer context, DNAAF2 knockout allows dissection of ciliary motility gene roles in tumor cell behavior. Although A2780 cells are not classically considered a ciliated model, they may possess primary cilia under certain conditions, and ciliary dysfunction can influence pathways such as Hedgehog or Wnt, potentially affecting proliferation, migration, or drug sensitivity. This model thus enables exploration of how ciliogenesis defects intersect with platinum-sensitive ovarian cancer phenotypes and may reveal novel roles for motile cilia genes in epithelial malignancies.
Typical research applications include modeling primary ciliary dyskinesia in an ovarian cancer background, studying the impact of ciliary gene disruption on cancer progression, and screening for ciliopathy therapeutics. Knockout validation can be performed by western blotting, RT-qPCR, and immunofluorescence for ciliary markers such as acetylated tubulin and ARL13B. Functional assays include flow cytometry for cilia detection, co-immunoprecipitation of dynein complex components, cisplatin sensitivity assays, and transcriptome analysis by RNA-seq to identify downstream targets. For further information, contact Ascent Research.
