The CCDC120 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human gastric adenocarcinoma AGS cell line, featuring targeted disruption of the CCDC120 gene. This gene-edited pool comprises a heterogeneous mix of knockout variants, providing a loss-of-function model for studying CCDC120-dependent signaling without clonal selection bias. The polyclonal format retains genetic diversity and is well-suited for pooled functional screens and population-level assays.
The AGS cell line, established from a diffuse-type gastric adenocarcinoma of a 54-year-old female patient, is a widely employed model in gastric cancer research. AGS cells exhibit epithelial morphology, adherent growth, and retain molecular features of gastric adenocarcinoma, including activation of growth factor signaling cascades. They are commonly used to investigate tumor cell proliferation, migration, and drug sensitivity. The integration of CCDC120 knockout into this well-characterized background enables precise dissection of scaffold protein functions in a gastric cancer-relevant cellular milieu.
CCDC120 encodes a scaffold protein that orchestrates AKT1 activation by assembling a signaling complex with PDK1 and the regulatory subunit PIK3R1 of PI3K. Upon stimulation by upstream factors such as EGF, PDGF, or IGF1, CCDC120 facilitates the colocalization of AKT1 with its activating kinases, promoting phosphorylation at Ser473 and subsequent full activation. Active AKT1 then phosphorylates downstream targets including GSK3B, mTOR, and p70S6K, which collectively regulate cell cycle progression, protein synthesis, and cytoskeletal dynamics. Consequently, CCDC120 functions as a critical enhancer of the PI3K/AKT signaling axis, driving cell migration and proliferation. Disruption of CCDC120 by CRISPR/Cas9 ablates this scaffolding function, leading to dampened AKT pathway activity and consequent impairment of cellular motility and growth.
In gastric adenocarcinoma, hyperactivation of the PI3K/AKT pathway is a frequent driver of tumor progression, metastasis, and therapeutic resistance. CCDC120 has been implicated in promoting aggressive phenotypes in gastric and breast cancers, making it a relevant target for mechanistic studies. The CCDC120 knockout AGS polyclonal cells thus constitute a physiologically appropriate model system to dissect how loss of this scaffold protein alters oncogenic signaling networks, reduces invasive capacity, and sensitizes cells to pathway-targeted agents. This model is particularly valuable for interrogating scaffold-dependent signaling vulnerabilities that may be exploited in precision oncology approaches.
Researchers can employ this knockout cell population in a variety of functional assays to dissect CCDC120 biology and screen for modulators of the PI3K/AKT pathway. Typical applications include evaluating phosphorylation status of AKT1 at Ser473 by Western blotting, assessing cell migration via transwell assays, measuring clonogenic survival and proliferation through colony formation and MTT assays, and visualizing cytoskeletal rearrangements with F-actin immunofluorescence. Additionally, live-cell imaging enables real-time tracking of motility defects. These cells support investigations into gastric cancer metastasis mechanisms, scaffold protein roles in signal transduction, and high-throughput screening of candidate PI3K/AKT inhibitors. For further information or technical support, please contact Ascent Research.
