The CCNT2 Knockout AGS Polyclonal Cells constitute a genetically heterogeneous population of AGS gastric adenocarcinoma cells in which the CCNT2 gene has been disrupted by CRISPR/Cas9-mediated gene editing. This polyclonal knockout cell pool avoids clonal bias and provides a robust loss-of-function model for studying CCNT2-dependent transcriptional regulation in a gastric cancer context. The product is supplied as a live cell mixture, ready for expansion and downstream functional assays, and no single-cell cloning has been performed.
The parental AGS cell line was originally derived from a poorly differentiated human gastric adenocarcinoma and displays typical epithelial morphology. It is extensively characterized as an in vitro model for gastric cancer research, including studies of oncogenic signaling, metastasis, and drug response. The gastric origin of AGS cells makes them particularly relevant for investigating molecular mechanisms that drive gastric tumorigenesis, such as aberrant transcriptional control and cell cycle dysregulation.
CCNT2 encodes cyclin T2, the regulatory subunit of P-TEFb, which activates CDK9 to phosphorylate serine 2 of the RNA polymerase II CTD, enabling promoter escape and productive elongation. P-TEFb is recruited by BRD4 and NF-??B, while its activity is suppressed by the 7SK snRNP containing HEXIM1, LARP7, and 7SK snRNA. HIV-1 Tat competitively displaces HEXIM1 to hijack P-TEFb for viral transcription. Downstream targets include FOS, JUN, MYC, and BCL2, which are regulated at the level of transcriptional elongation.
Knockout of CCNT2 in AGS gastric cancer cells disrupts P-TEFb-dependent transcription of genes that sustain proliferation and survival. This model therefore allows investigation of how elongation control contributes to gastric cancer phenotypes, including responses to NF-??B-driven inflammatory signals and BRD4-mediated chromatin regulation. Given the role of CDK9 in oncogenic transcription, the CCNT2 knockout AGS pool is useful for studying the consequences of impaired elongation on gastric cancer cell growth and apoptosis.
These cells are suitable for transcriptomic analyses (RNA-seq, RT-qPCR), ChIP assays assessing RNA polymerase II occupancy, and co-immunoprecipitation studies of P-TEFb complex formation. Drug screening with CDK9 inhibitors and HIV LTR-based reporter assays can measure functional consequences of CCNT2 loss. Standard cell proliferation and apoptosis assays further characterize the impact on gastric cancer cell fitness. For additional information or technical assistance, please contact Ascent Research.
