The CCNYL1 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population generated from the human HT29 colorectal adenocarcinoma cell line. This product delivers a heterogeneous pool of cells with targeted CCNYL1 gene disruption, providing a versatile loss-of-function model for studying cyclin biology in cancer. The polyclonal nature minimizes clonal artifacts and makes the population suitable for high-throughput screening and pooled functional assays.
HT29 is a widely used adherent epithelial cell line originally derived from a 44-year-old Caucasian female with colorectal adenocarcinoma. It retains key properties of intestinal epithelium, including the ability to form polarized monolayers and express tight junction proteins, making it a standard model for colorectal cancer research, barrier function studies, and drug absorption analysis. This well-characterized background facilitates direct comparison with wild-type HT29 data and supports integrative pathway analysis.
CCNYL1 encodes a cyclin protein that is predicted to bind and activate cyclin-dependent kinases, including CDK14, to promote cell cycle progression. Its function is controlled by upstream signals such as E2F1 transcription factor, MAPK1, and AKT1, and it contributes to the expression of CCND1 and the phosphorylation of RB1, ultimately driving E2F1-mediated transcription. Negative regulation occurs through interactions with the CDK inhibitors CDKN1A (p21) and CDKN1B (p27). Thus, CCNYL1 integrates proliferative and inhibitory cues to modulate G1/S transition in colorectal cancer cells.
Knockout of CCNYL1 in HT29 cells is expected to impair proliferation and induce cell cycle arrest, particularly at the G1 phase, by disrupting cyclin-CDK signaling networks that are commonly dysregulated in colorectal tumors. The model??s value is heightened by the HT29 genetic background, which includes APC and TP53 mutations, as loss of CCNYL1 may expose synthetic vulnerabilities or enhance sensitivity to chemotherapeutics, offering a platform for exploring targeted therapy strategies.
These polyclonal knockout cells are well-suited for a range of applications, including MTT or BrdU proliferation assays, cell cycle flow cytometry, Western blotting for cyclin and CDK levels, colony formation assays, and RT-qPCR for cell cycle gene expression. They enable functional dissection of cyclin-CDK pathways, drug target validation, and identification of compounds that differentially affect CCNYL1-deficient cells. For technical support and custom genome editing services, please contact Ascent Research.
