The CCDC6 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the CCDC6 tumor suppressor gene in the Jurkat T lymphocyte line. This loss-of-function model facilitates unbiased functional study of CCDC6-dependent processes without clonal selection artifacts, offering a pooled knockout background ideal for research in cancer biology and DNA damage signaling. The cells are generated via CRISPR/Cas9-mediated gene disruption, providing a heterogeneous population for robust phenotypic analysis.
The Jurkat host line originates from a 14-year-old male with relapsed acute T-cell leukemia and expresses CD3, CD4, and IL-2 receptor, serving as a widely used model for T-cell receptor signaling and acute lymphoblastic leukemia. Its leukemic background, characterized by dysregulated proliferation and survival, enables detailed investigation of oncogenic pathways and tumor suppressor mechanisms directly relevant to hematological malignancies and immune cell signaling.
CCDC6 is a tumor suppressor that mediates DNA damage-induced apoptosis through the ATM-p53 axis. Upon genotoxic stress, ATM kinase phosphorylates CCDC6, which interacts with USP7 to modulate p53 stability, thereby promoting transcription of pro-apoptotic factors BAX and PUMA and triggering caspase activation. CCDC6 also associates with CREB1 to influence CREB-mediated transcriptional programs and with PP4C in DNA repair contexts, integrating DNA damage signals with cell cycle arrest and cell death decisions. Its involvement in MAPK signaling further underscores its multifunctional role in cellular stress responses.
In Jurkat cells, CCDC6 knockout attenuates apoptosis induced by DNA-damaging agents such as etoposide and doxorubicin, enhancing survival and modeling therapeutic resistance. Wild-type Jurkat cells exhibit altered apoptotic thresholds despite intact p53, and CCDC6 loss further impairs caspase-dependent cell death, providing insights into leukemogenesis and tumor suppressor loss in T-cell malignancies. This model allows precise dissection of CCDC6??s interactions with USP7 and CREB1 in a disease-relevant environment and offers a platform for evaluating chemosensitivity.
Researchers can apply these polyclonal cells in flow cytometry for apoptosis and cell cycle analysis, Western blotting for cleaved caspase-3 and p53, immunofluorescence for ??-H2AX foci, and co-immunoprecipitation to confirm CCDC6-USP7 complexes. RT-qPCR profiling of p53 target genes and drug sensitivity screens with doxorubicin or etoposide reveal CCDC6-dependent chemoresistance. Applications extend to thyroid cancer research, leukemia survival pathway dissection, and high-throughput genetic screens. For further information, please contact Ascent Research.
