The HNF4A Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the gene encoding hepatocyte nuclear factor 4 alpha (HNF4A) has been disrupted within the human A2780 ovarian epithelial adenocarcinoma cell line. This loss-of-function model is supplied as a heterogeneous pool of edited cells, enabling researchers to interrogate HNF4A-dependent signaling in the context of ovarian carcinoma without relying on single-cell-derived clonal isolation.
The A2780 parental cell line is a well-characterized human ovarian carcinoma model exhibiting epithelial morphology, originally established from an untreated patient and widely employed in studies of chemotherapy response, particularly platinum-based drug sensitivity and resistance mechanisms. Its epithelial origin and genetic background make it an appropriate host for examining transcription factors governing epithelial identity and metabolism.
HNF4A is a master transcriptional regulator belonging to the nuclear receptor superfamily and is critical for hepatocyte differentiation and epithelial morphogenesis. It transcriptionally activates a network of target genes including CYP3A4, ABCB1, ALB, CLDN1, OCLN, and HNF1A, which are essential for drug metabolism, tight junction assembly, and maintenance of cellular polarity. HNF4A activity is modulated by upstream factors such as HNF1??, FOXA2, GATA4, the glucocorticoid receptor NR3C1, miR-34a, and CREB1, and it exerts its transcriptional effects through interactions with cofactors including RXRA, PPARGC1A, NCOA1, NCOR1, SMAD3, and CREBBP. The HNF4A-HNF1A-FOXA2 regulatory axis integrates inputs from Wnt/??-catenin and TGF-?? pathways to govern epithelial differentiation programs.
In A2780 ovarian cancer cells, disruption of HNF4A is expected to impair epithelial junction integrity and alter the expression of genes involved in xenobiotic metabolism, thereby potentially modifying cellular responses to chemotherapeutic agents. This model enables investigation of HNF4A’s role in epithelial-mesenchymal transition (EMT), metabolic reprogramming, and the interplay between transcriptional regulation and drug resistance in ovarian carcinoma, where HNF4A expression patterns have been correlated with tumor progression and patient outcomes.
Researchers can utilize this polyclonal knockout cell population in a broad range of assays, including RNA sequencing to map HNF4A-dependent transcriptomes, ChIP-seq for target gene identification, immunoblotting and RT-qPCR for validation, immunofluorescence staining of tight junction markers such as CLDN1 and OCLN, flow cytometry-based cell cycle and apoptosis analyses, transwell migration and invasion experiments, and drug sensitivity profiling using cisplatin or other chemotherapeutics. High-throughput drug screening and reporter gene assays further expand the model’s utility in functional genomics and pharmacology studies. For further technical information, please contact Ascent Research.
