CCL21 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma HeLa cell line. This product provides a heterogeneous population of cells with targeted disruption of the CCL21 gene, generated by CRISPR/Cas9-mediated gene editing. The polyclonal format ensures a diverse representation of knockout genotypes across the cell population, enabling robust functional studies without the limitations of single-cell clonal selection.
The HeLa host cell line is an epithelial cell model originally isolated from a cervical adenocarcinoma. HeLa cells are positive for human papillomavirus type 18 (HPV-18) and exhibit p53 degradation mediated by the viral E6 oncoprotein and retinoblastoma protein (Rb) inactivation by E7. This background renders HeLa cells immortalized and widely used for investigating fundamental cell biology, oncogenic transformation, and signaling pathways in a human epithelial context.
The CCL21 gene encodes the homeostatic chemokine C-C motif chemokine ligand 21, a key regulator of immune cell trafficking. CCL21 primarily signals through the chemokine receptor CCR7, which is expressed on lymphocytes, dendritic cells, and natural killer cells. Upon ligand binding, CCR7 activates G-protein-dependent cascades, including PI3K/AKT and MAPK/ERK pathways, as well as Rho GTPases such as Rac1 and Cdc42, leading to cytoskeletal rearrangement and directed cell migration. Upstream regulators of CCL21 expression include tumor necrosis factor-alpha (TNF-??), interleukin-1 beta (IL-1??), and NF-??B, while downstream mediators involve ??-arrestin and JAK/STAT signaling. Additionally, ACKR4 (CCRL1) functions as a scavenger receptor for CCL21, modulating its extracellular gradient.
In the HeLa cell context, CCL21 knockout disrupts the autocrine or paracrine signaling that may influence tumor?Cimmune interactions. Although HeLa cells are not professional immune cells, they can express chemokines upon inflammatory stimuli, contributing to the tumor microenvironment. Loss of CCL21 impairs the ability to attract CCR7-expressing immune cells, thereby altering immune surveillance and potentially affecting metastatic behavior. This model thus provides a valuable tool to dissect the role of chemokine signaling in epithelial tumor biology and immune evasion strategies.
Typical research applications include cancer immunology studies, chemotaxis and migration assays, and drug discovery targeting the CCL21/CCR7 axis. The polyclonal knockout cells are suitable for Transwell migration assays, wound healing experiments, flow cytometric analysis of CCR7 expression, and Western blotting for downstream signaling components such as phosphorylated AKT and ERK. Further, these cells can be employed in co-culture systems to model immune cell recruitment and in high-throughput screening for CCR7 antagonists. For additional details, please contact Ascent Research.
