The CCL7 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma line, engineered for disruption of the CCL7 gene. This heterogeneous knockout model provides a loss-of-function system to study CCL7 biology without the selective pressure of single-cell cloning, enabling robust representation of gene disruption effects across a mixed cellular background. It is suitable for pooled functional screens, bulk biochemical assays, and experiments requiring diverse allelic variation to reflect population-level responses.
HGC-27 is an epithelial cell line originally isolated from a metastatic lymph node of a human signet ring cell gastric adenocarcinoma. It is widely utilized as a model for gastric cancer metastasis, invasion, and tumor-stroma interactions due to its aggressive characteristics and retention of key molecular features of advanced disease. The cell line??s established use in cancer biology makes it a relevant platform for interrogating genes involved in tumor progression and the immune microenvironment.
CCL7 encodes a CC chemokine that directs the trafficking of monocytes, T cells, eosinophils, and basophils to inflammatory sites by binding to chemokine receptors CCR1, CCR2, and CCR3. Receptor engagement triggers G-protein?Ccoupled signaling cascades, activating MAPK/ERK and PI3K/AKT pathways, which in turn promote calcium influx, integrin activation, and MMP-9 secretion. CCL7 expression is upregulated by proinflammatory mediators including TNF-??, IL-1, IFN-??, and LPS through NF-??B activation. Downstream, CCL7 signaling interfaces with effector molecules such as PLC, MAPK, PI3K, and JAK/STAT, while interactions with glycosaminoglycans and matrix metalloproteinases modulate its localization and activity.
In gastric cancer, CCL7 is implicated in promoting metastasis by recruiting tumor-associated macrophages and inducing MMP-dependent extracellular matrix remodeling, thereby facilitating cancer cell invasion. The knockout of CCL7 in HGC-27 cells allows researchers to dissect these mechanisms and examine how loss of this chemokine alters tumor cell migration, immune cell crosstalk, and signaling through NF-??B or JAK/STAT pathways. This model is particularly valuable for exploring the interplay between chronic inflammation and malignant progression in a gastric adenocarcinoma context.
Typical research applications include Transwell migration and invasion assays to quantify metastatic potential, co-culture systems with immune cells to evaluate tumor-immune interactions, and phospho-kinase arrays or RNA-seq to profile downstream pathway alterations. ELISA and flow cytometry enable measurement of chemokine secretion and receptor expression, while Western blotting and RT-qPCR confirm target disruption and signaling node activity. The polyclonal knockout format is well-suited for high-content screening, anti-inflammatory drug target validation, and detailed mechanistic studies of CCL7 function in gastric cancer. For further technical details or to order this product, please contact Ascent Research.
