The CCL7 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, designed to disrupt the gene encoding chemokine (C-C motif) ligand 7 (CCL7). This product provides a heterogeneous pool of gene-edited cells, enabling functional loss-of-function studies without the selection of a single clonal isolate. The polyclonal format preserves genetic diversity while ensuring targeted disruption of CCL7, allowing researchers to assess the collective impact of gene ablation on cellular phenotypes and signaling networks.
The parental A2780 cell line is an established epithelial ovarian cancer model isolated from an untreated patient, widely utilized in ovarian cancer research and drug resistance investigations. A2780 cells exhibit characteristic features of high-grade serous ovarian carcinoma and serve as a robust platform for studying oncogenic signaling, chemosensitivity, and tumor cell behavior. Their use in generating this knockout pool provides a clinically relevant background for exploring CCL7 function in ovarian malignancy.
CCL7 functions as a broad-spectrum chemoattractant, binding to chemokine receptors CCR1, CCR2, and CCR3, and glycosaminoglycans, to orchestrate directed migration of monocytes, dendritic cells, T cells, and basophils. Ligand-receptor engagement activates G protein-coupled signaling cascades, predominantly the PI3K/AKT and MAPK/ERK pathways, which phosphorylate downstream effectors such as FAK and promote expression of matrix metalloproteinases (MMPs). Transcription of CCL7 is regulated by inflammatory stimuli, including TNF??, IL-1??, and IFN-??, through transcription factors NF-??B and AP-1. Consequently, CCL7 integrates extracellular inflammatory cues with intracellular migratory and survival signals, positioning it at the nexus of immune cell recruitment and tissue remodeling.
In the context of ovarian carcinoma, CCL7-mediated chemotaxis may contribute to the composition of the tumor microenvironment by recruiting immune cells that can either suppress or promote tumor progression. Disruption of CCL7 in A2780 cells is expected to impair autocrine and paracrine chemokine signaling, potentially altering tumor-immune cell crosstalk, reducing matrix degradation via MMP downregulation, and affecting pathways linked to metastasis. This knockout model thus enables dissection of CCL7-specific roles in ovarian cancer cell migration, invasion, and immunomodulatory functions.
Typical research applications include investigating tumor-immune microenvironment interactions, ovarian cancer metastasis, chemokine signaling dynamics, and inflammation-driven carcinogenesis. The pool of knockout cells is amenable to an array of experimental techniques such as Boyden chamber migration assays to quantify directional motility, calcium flux assays to measure rapid receptor activation, ELISA for secreted CCL7 quantification, western blotting for phospho-AKT and phospho-ERK, RT-qPCR for transcript analysis of CCL7 and downstream targets, and flow cytometry for profiling chemokine receptor surface expression. For additional technical specifications or batch-specific data, please contact Ascent Research.
