The ATAD2 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cervical adenocarcinoma cell line. This heterogeneous pool of genetically modified cells provides a physiologically relevant loss-of-function model for investigating ATAD2 (ATPase family AAA domain-containing protein 2), avoiding artifacts associated with clonal selection. The knockout cell population was generated through CRISPR/Cas9-mediated gene disruption of the ATAD2 locus, enabling robust functional studies while preserving the genetic background of the parental HeLa cell line.
HeLa cells are a widely utilized human cell line originally isolated from a cervical adenocarcinoma and are positive for human papillomavirus type 18 (HPV18). As an immortalized epithelial cancer cell line, HeLa cells serve as a standard platform for cancer biology research, particularly in studies of tumor cell proliferation, viral oncoprotein interactions, and therapeutic development. Their ease of culture, consistent growth characteristics, and extensive characterization make them an ideal host for gene-editing applications, including the interrogation of oncogenic transcriptional regulators such as ATAD2.
ATAD2 is a key transcriptional coactivator and chromatin remodeler that integrates signals from estrogen, androgens, and MYC to drive proliferation and survival. It directly interacts with nuclear hormone receptors ER?? and AR, as well as MYC and E2F transcription factors, and couples with the NuRD remodeling complex to establish active chromatin at target gene promoters. Critical downstream effectors include Cyclin D1, a cell cycle promoter, and BIRC5 (Survivin), an apoptosis inhibitor. This positions ATAD2 as a central node in oncogenic transcriptional networks.
In the HeLa cervical cancer context, this ATAD2 knockout model enables dissection of its specific contributions to malignant phenotypes. Since ATAD2 is frequently overexpressed in cervical, breast, prostate, and other hormone-responsive cancers, disrupting its function in an HPV-positive adenocarcinoma background allows researchers to examine cross-talk between viral oncoproteins, steroid hormone signaling, and MYC-dependent transcription. The polyclonal population mitigates clonal bias, offering a more representative view of ATAD2-dependent effects on proliferation, cell cycle progression, and apoptotic resistance, which are hallmarks of cervical carcinogenesis.
This product is suited for proliferation assays (e.g., CellTiter-Glo), apoptosis testing, RT-qPCR for Cyclin D1 and BIRC5, Western blotting, ChIP, and reporter gene assays. It enables cancer proliferation studies, transcriptional regulation analysis, drug target validation, and hormone signaling research in breast, prostate, lung, ovarian, and cervical cancer models. For further technical details or assistance with experimental design, please contact Ascent Research.
