The CCDC6 Knockout AGS Polyclonal Cells product provides a CRISPR/Cas9-edited heterogeneous population of the AGS human gastric adenocarcinoma cell line carrying targeted disruption of the CCDC6 tumor suppressor gene. This polyclonal knockout pool serves as a diverse loss-of-function model suitable for investigating CCDC6 roles in DNA damage response and apoptosis without the constraints of clonal selection. The polyclonal nature allows for population-level analyses such as drug sensitivity screening and pooled functional assays, reflecting the genetic variability present in edited cell populations.
The AGS cell line was originally isolated from the gastric adenocarcinoma tissue of a 54-year-old Caucasian female and is widely employed in gastric cancer research. As an epithelial adherent line derived from a primary tumor, AGS retains key signaling and growth properties of gastric adenocarcinoma, providing a clinically relevant background for studying tumor suppressor gene function. The cell line??s well-characterized behavior in DNA damage and apoptosis assays makes it a robust host for knockout studies targeting genome maintenance factors.
CCDC6 functions as a critical tumor suppressor at the intersection of DNA repair and cell death pathways. Upon genotoxic insult, the ATM kinase phosphorylates CCDC6, promoting its interaction with the phosphatase PP4C and the DNA repair kinase DNA-PKcs, thereby modulating non-homologous end joining. CCDC6 also engages the transcriptional coactivator CREB1 and contributes to p53-dependent apoptotic signaling, placing it within the ATM?C??H2AX?C53BP1?Cp53 axis. Loss of CCDC6 attenuates DNA damage-induced phosphorylation of ??H2AX and 53BP1 and impairs apoptosis execution, thereby fostering genomic instability.
In the context of AGS gastric adenocarcinoma cells, CCDC6 disruption recapitulates DDR deficiencies that are hallmarks of gastric tumorigenesis. This polyclonal knockout model enables researchers to dissect how heterogeneous CCDC6 loss impacts cellular responses to ionizing radiation and chemotherapeutic agents, shedding light on treatment resistance mechanisms. The system is thus uniquely suited for genotype-phenotype correlation studies that explore the functional consequences of tumor suppressor inactivation in gastric cancer cells.
Researchers can utilize this polyclonal knockout pool in a range of experimental approaches, including western blotting for CCDC6 and DNA double-strand break markers, immunofluorescence visualization of ??H2AX foci, and cell viability or apoptosis assays following DNA damage induction. Further applications encompass colony formation assays to assess proliferative capacity, RT-qPCR for downstream target quantification, comet assays for direct DNA damage measurement, and drug sensitivity profiling to identify synthetic lethal interactions. For further information or to discuss how this product can support your research, please contact Ascent Research.
