The CCDC6 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cervical adenocarcinoma line. This product provides a loss-of-function model for the tumor suppressor gene CCDC6, which is critical in DNA damage response, apoptosis, and transcriptional control.
HeLa cells, an immortalized epithelial cell line originally derived from a cervical adenocarcinoma, are positive for human papillomavirus type 18 (HPV18). They are extensively utilized in cancer biology, signal transduction, and gene expression research, particularly for dissecting cervical cancer mechanisms. Their robust and well-characterized nature makes them a suitable host for CRISPR/Cas9-mediated gene disruption studies.
CCDC6 functions as a tumor suppressor by acting as a scaffold for a phosphatase-deacetylase complex comprising PP4C and HDAC1. This complex dephosphorylates and deacetylates CREB1, keeping CREB in a repressed state that limits transcription of pro-survival genes such as BCL2 and c-FOS. Upon DNA damage, the kinases ATM and ATR phosphorylate CCDC6, causing complex disassembly and consequent activation of CREB, which promotes expression of apoptotic and cell cycle arrest genes. Additionally, CCDC6 interacts with 14-3-3 proteins and influences downstream targets like p21, thereby integrating signaling pathways that regulate cell cycle progression and centrosome integrity. Disruption of this network can lead to aberrant cell survival and genomic instability.
In the HeLa cervical adenocarcinoma background, CCDC6 knockout serves as a powerful tool to investigate tumor suppressor loss. CCDC6 alterations are frequently observed in papillary thyroid carcinoma, non-small cell lung cancer, breast cancer, and ovarian cancer. This polyclonal knockout population, harboring a heterogeneous mix of CCDC6-disrupted cells, models the variability found in tumors and enables examination of how abrogation of the ATM/ATR-CCDC6-CREB axis contributes to defective apoptosis, centrosome abnormalities, and unchecked proliferation in cervical cancer.
This model supports a wide range of experimental applications. Researchers can perform western blotting for CCDC6 and phospho-CREB; RT-qPCR for CREB target genes (BCL2, c-FOS); annexin V/propidium iodide apoptosis assays in response to cisplatin; immunofluorescence for centrosome markers; cell viability and CREB luciferase reporter assays; and co-immunoprecipitation to probe interactions with HDAC1, PP4C, and 14-3-3. For further technical support, contact Ascent Research.
