The KDM4A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cervical adenocarcinoma cell line. This heterogeneous pool carries targeted disruptions in the KDM4A gene, enabling loss-of-function studies without clonal bias. The polyclonal format provides a broad representation of KDM4A ablation, ideal for epigenetic and DNA damage response research in a cervical cancer context.
HeLa cells are an immortalized human cervical epithelial adenocarcinoma line, originally from an HPV18-positive adenocarcinoma. They feature inactivation of p53 and Rb via HPV E6 and E7 oncoproteins, fostering uncontrolled proliferation. This background makes HeLa a robust model for cancer biology and CRISPR-based editing, supporting reproducible functional assays.
KDM4A (JMJD2A) is a histone lysine demethylase that removes methyl groups from H3K9me2/3 and H3K36me2/3, influencing chromatin accessibility and transcriptional regulation. It functions downstream of HIF1A, ATM/ATR-mediated DNA damage signals, and oncogenic RAS, while being targeted by miR-137. KDM4A interacts with chromatin modifiers and repair factors including HP1??, the NuRD complex, PARP1, HDAC1, and PRMT5. By demethylating histone marks at promoters of MYC and CCND1, KDM4A facilitates their transcriptional activation, driving proliferation and tumorigenesis. In HeLa cells, abrogation of KDM4A function disrupts this network, impairing DNA repair and heightening sensitivity to genotoxic agents like etoposide.
In the HeLa background, KDM4A knockout uncouples histone demethylation from the HPV-driven inactivation of p53 and Rb, enabling study of epigenetic drivers in cervical carcinogenesis. This model is particularly suited for examining how KDM4A sustains proliferation and DNA damage resistance in the context of oncogenic stress. It also allows dissection of KDM4A-dependent modulation of hypoxia signaling and its crosstalk with PARP1 and ATM/ATR pathways.
Applications include ChIP-qPCR for histone modification profiling, RT-qPCR for MYC and CCND1 expression, and MTT/BrdU proliferation assays. DNA damage responses can be monitored via ??H2AX immunofluorescence, complemented by drug sensitivity testing with etoposide. The polyclonal knockout population supports epigenetic drug screens and target validation in cervical cancer. For additional inquiries, please contact Ascent Research.
