The CCR9 knockout A-549 polyclonal cells are a CRISPR/Cas9-edited population of human lung adenocarcinoma cells with targeted disruption of the CCR9 gene. This polyclonal pool, generated without clonal isolation, provides a loss-of-function model suitable for bulk functional studies, avoiding clonal biases while maintaining the biological variability of an edited cell population. The product enables investigation of CCR9-dependent signaling and metastatic behavior in a well-characterized lung cancer background.
The A-549 cell line, derived from a 58-year-old male with lung adenocarcinoma, is a classic model for alveolar type II epithelium and is widely used in cancer research. It carries an activating KRAS mutation and retains wild-type p53, recapitulating common genetic features of non-small cell lung cancer. These cells are robust for in vitro assays of migration, invasion, and drug response, providing a relevant context for studying chemokine receptor functions.
CCR9 is a G??i-coupled receptor for the chemokine CCL25, primarily known for directing lymphocyte homing to the gut. In cancer, the CCL25-CCR9 axis activates PI3K/Akt and MAPK/ERK cascades, promoting survival and proliferation, and stimulates FAK and integrin ??4??7 to enhance adhesion and migration. Upstream regulators include GATA3 and inflammatory cytokines TNF-?? and IL-1??, while downstream effectors encompass phosphorylated Akt, ERK1/2, c-Myc, and cyclin D1. ??-arrestin mediates receptor desensitization and contributes to signaling diversity.
Disruption of CCR9 in A-549 cells abrogates CCL25-induced chemotaxis and adhesion by eliminating downstream phosphorylation of Akt, ERK1/2, and FAK. This knockout model therefore allows direct assessment of CCR9??s contribution to lung adenocarcinoma metastasis, independent of other chemokine systems. The KRAS-mutant background further enables analysis of potential crosstalk between CCR9 and oncogenic signaling, offering a platform to evaluate whether targeting this receptor can impair tumor migration and survival.
This polyclonal knockout product is intended for applications such as Transwell migration and Matrigel invasion assays using CCL25 gradients, Western blot detection of p-Akt and p-ERK, flow cytometry for integrin ??4??7, and qPCR for CCR9 transcript levels. It supports research on inflammatory bowel disease, colorectal cancer, and T-cell lymphoma, with particular relevance to studies of lung cancer metastasis and chemokine-directed therapy. For inquiries or custom services, please contact Ascent Research.
