In Stock Cell Lines
Homo sapiens (Human)
Ovary
Adherent and suspension
The PUS7 Knockout A2780 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the A2780 human ovarian carcinoma line, offering a loss?of?function model for the RNA pseudouridine synthase PUS7. This line is ideal for investigating epitranscriptomic regulation in ovarian cancer, as PUS7 catalyzes pseudouridylation of tRNA and mRNA to enhance MYC?driven translation and tumor growth. Applications include pseudouridine sequencing, polysome profiling, and drug resistance studies. Key signaling interactions involve MYC, mTORC1, and WNT/???catenin pathways, with downstream effects on tRNA?Leu and MYC target gene expression.
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The PUS7 Knockout A2780 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the A2780 human ovarian carcinoma line, in which the PUS7 gene has been functionally disrupted to create a loss?of?function model. This product provides a genetically defined system for studying the roles of pseudouridine modification in cancer biology.
The A2780 cell line is a widely used epithelial ovarian carcinoma model established from an untreated patient. It retains cisplatin sensitivity and robust tumorigenicity, making it particularly relevant for investigating ovarian cancer pathogenesis and mechanisms underlying chemotherapeutic response.
PUS7 encodes a pseudouridine synthase that catalyzes the isomerization of uridine to pseudouridine on specific tRNA substrates, including tRNA?Leu and tRNA?Lys, as well as on MYC mRNA. This modification enhances translation efficiency of MYC?dependent mRNAs, thereby promoting oncogenic protein synthesis. PUS7 is regulated by upstream signals such as MYC proto?oncogene protein, mTORC1, and WNT/???catenin signaling, and it interacts with translation initiation factors like eIF4E within a network that includes TCF/LEF transcription factors.
Knockout of PUS7 in the A2780 background disrupts pseudouridylation, leading to impaired translation of MYC and its target genes (e.g., CCND1 and ribosomal proteins). This results in reduced proliferation, diminished stem cell self?renewal, and attenuated tumorigenic potential. The model is thus instrumental for dissecting the epitranscriptomic control of the MYC?CmTOR axis and for probing determinants of cisplatin resistance.
This knockout cell line supports diverse research applications, including pseudouridine sequencing to identify modification targets, polysome profiling to assess translational regulation, and functional assays such as colony formation, apoptosis, and xenograft models. It is also suitable for CRISPR screening to uncover synthetic lethal interactions and for exploring therapeutic vulnerabilities in ovarian cancer. For further details or to inquire about this product, please contact Ascent Research.
