The CCL7 Knockout KYSE-30 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the KYSE-30 human esophageal squamous cell carcinoma line, featuring targeted disruption of the CCL7 gene. This product offers a versatile loss-of-function model for functional studies of the CCL7-encoded chemokine. The polyclonal knockout configuration minimizes clonal selection bias, providing a heterogeneous cell pool that better represents the genetic diversity of the parental line. This format is well-suited for assays requiring stable gene knockout without the artifacts associated with single-cell cloning.
KYSE-30 is an epithelial, well-differentiated esophageal squamous cell carcinoma line originally isolated from a 64-year-old male primary tumor. It is extensively used to investigate esophageal cancer mechanisms, including tumor growth, invasion, and response to therapies. The cell line retains key characteristics of esophageal squamous cell carcinoma, making it a relevant host for studying chemokine-mediated processes in this malignancy. Its defined background supports reproducible experimentation in cancer biology.
The CCL7 gene encodes a chemokine critical for recruiting monocytes and eosinophils. It binds to receptors CCR1, CCR2, and CCR3, activating downstream G protein-coupled signaling cascades that include phospholipase C, PI3K, and MAPK/ERK pathways. Expression of CCL7 is transcriptionally regulated by TNF-alpha, IL-1??, IFN-gamma, and NF-??B. Once induced, CCL7 promotes cell migration and modulates inflammatory responses via interactions with cytokines and glycosaminoglycans, linking it to pathways such as JAK-STAT and NF-kappa B signaling.
In esophageal squamous cell carcinoma, CCL7 is thought to contribute to tumor progression by facilitating leukocyte migration and shaping the tumor microenvironment. KYSE-30 cells express components of chemokine signaling networks, making the CCL7 knockout in this background a valuable tool for dissecting autocrine and paracrine effects. Disruption of CCL7 can affect cancer cell motility, invasion, and immune cell recruitment, offering insights into the interplay between inflammation and esophageal cancer.
This polyclonal knockout model supports diverse applications, including transwell migration assays, ELISA, Western blot, RT-qPCR, flow cytometry, cell viability tests, and immunohistochemistry. It is ideal for studying esophageal cancer biology, chemokine signaling, tumor microenvironment dynamics, immune cell recruitment, and drug target validation. The heterogeneous knockout population allows examination of mixed cellular responses. For additional product details, please contact Ascent Research.
