The CCNT2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of A2780 human ovarian adenocarcinoma cells with targeted disruption of the CCNT2 gene. As a polyclonal pool, this product provides a heterogeneous allele mixture suitable for loss-of-function studies without monoclonal isolation. CRISPR/Cas9 gene editing ensures efficient targeting while preserving the parental A2780 background, offering a physiologically relevant model for examining Cyclin T2 depletion in ovarian cancer.
A2780 cells are an epithelial cell line derived from an untreated ovarian cancer patient, characterized by cisplatin sensitivity and well-defined growth properties. This chemotherapy-na?ve model retains key signaling pathways often altered in resistant disease, making it ideal for investigating intrinsic drug responses and tumor suppressors. The parental line supports robust proliferation and accepts diverse downstream analyses, including proliferation assays and transcriptomic profiling.
CCNT2 encodes Cyclin T2, the regulatory subunit of P-TEFb, which with CDK9 phosphorylates RNA polymerase II CTD at Ser2 and inactivates DSIF and NELF, promoting transcriptional elongation. Cyclin T2 is regulated by NF-??B, BRD4, and the 7SK/HEXIM1 complex, and repressed by miR-198. Active P-TEFb drives expression of MYC, FOS, and BCL2, and facilitates HIV Tat-mediated LTR transactivation via interactions with Tat and AFF4. Thus, CCNT2 integrates signals to control proliferation, survival, and viral transcription.
In A2780 cells, CCNT2 knockout dissects P-TEFb’s role in oncogenic transcription. Ovarian cancers often rely on MYC and anti-apoptotic programs downstream of Cyclin T2. Disruption may reduce these effectors and sensitize to cisplatin. The polyclonal knockout allows comparison to wild-type A2780, linking changes in proliferation or drug response to Cyclin T2 loss, valuable for studying transcriptional elongation dependencies and therapeutic vulnerabilities.
Researchers can use these cells for RNA-seq and ChIP-qPCR to map transcriptional changes and Pol II occupancy upon CCNT2 depletion. Co-immunoprecipitation and western blotting confirm P-TEFb complex status. Cell proliferation and viability assays under cisplatin treatment can assess chemosensitization. The model also supports HIV LTR reporter assays to study Cyclin T2 in Tat-dependent transcription. Together, these applications make the cells a robust tool for cancer and HIV research. For further information, contact Ascent Research.
