Genome-edited Cells
Uterus (cervix)
The NAT10 Knockout SiHa Cell Line is a CRISPR/Cas9-edited human cervical cancer cell line with disruption of the NAT10 gene, which encodes an RNA acetyltransferase essential for rRNA and mRNA ac4C modification. This HPV-16-positive epithelial cell model allows interrogation of NAT10's functions in ribosome biogenesis, translation, and DNA damage response. Applications include studying ac4C-mediated oncogene translation, drug target validation, and cisplatin sensitivity assays. NAT10 interacts with UTP23 and NPM1 and is regulated by p53 and mTOR signaling. The line supports RNA-seq, ribosome profiling, proliferation, and apoptosis analyses.
PDIA6 Knockout A2780 Polyclonal Cells
Cat. No. ARG18841
CLCN2 Knockout HT29 Polyclonal Cells
Cat. No. ARG14694
ASF1A Knockout AGS Polyclonal Cells
Cat. No. ARG26668
PCED1B Knockout Hela Polyclonal Cells
Cat. No. ARG7743
PANK2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6446
CHD2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG3565
The NAT10 Knockout SiHa Cell Line is a human CRISPR/Cas9-edited knockout cell line designed for loss-of-function studies of NAT10, the gene encoding N-acetyltransferase 10. This stable cell line harbors a targeted disruption of the NAT10 gene, providing a versatile model system to investigate the biological functions of NAT10 and its role in disease.
The SiHa host cell line is an adherent epithelial cell line derived from a human cervical squamous cell carcinoma. SiHa cells contain integrated human papillomavirus type 16 (HPV-16) genomes and are a widely used model for studying cervical cancer biology, including tumor progression, metastasis, and response to therapeutic agents. Their HPV-positive status renders them particularly relevant for studying viral oncogene interactions with host cellular pathways.
NAT10 is an RNA cytidine acetyltransferase that catalyzes the formation of N4-acetylcytidine (ac4C) on rRNA and mRNA. Through this modification, NAT10 enhances RNA stability and promotes efficient translation. NAT10 functions in ribosome biogenesis by acetylating 18S and 28S rRNAs and interacts with UTP23, NPM1, RRN3, and TAF1B, as well as RNA polymerase I components. Upstream, NAT10 is regulated by p53, MYC, HIF1??, and mTOR signaling. Its downstream targets include cell cycle-related and pro-survival mRNAs. Thus, NAT10 sits at a nexus of RNA metabolism, translation control, and DNA damage responses.
In the SiHa cervical carcinoma background, NAT10 disruption is expected to impair ribosome production and mRNA translation, particularly of oncogenic transcripts stabilized by ac4C modification. This can lead to reduced cell proliferation and increased sensitivity to DNA-damaging agents, such as cisplatin. The knockout model therefore provides a valuable tool to dissect how ac4C modifications influence HPV-driven carcinogenesis and to identify synthetic lethal vulnerabilities that may be exploited therapeutically.
This NAT10 Knockout SiHa Cell Line is suitable for a range of research applications, including the study of RNA modifications in cervical cancer, ac4C-mediated oncogene translation, drug target validation, and DNA damage response assays. It can be used in synthetic lethal screening and in functional assays such as western blotting, RT-qPCR, RNA-seq, ribosome profiling, MTT and colony formation assays, annexin V staining, ??H2AX immunofluorescence, migration assays, and cisplatin sensitivity testing. For further details or to discuss your specific project needs, please contact Ascent Research.
