The CD47 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line. This product provides a loss-of-function model for CD47, a transmembrane protein that serves as a critical immune checkpoint by inhibiting phagocytic elimination. The polyclonal format ensures a heterogeneous pool of cells harboring diverse disruptive edits, allowing researchers to study the collective impact of CD47 disruption without the constraints of single-clone selection.
The HeLa host cell line is an immortalized epithelial cell line originating from a human cervical adenocarcinoma and is positive for human papillomavirus type 18 (HPV18). HeLa cells are highly proliferative and constitute one of the most widely used models in cancer biology, cell cycle research, and signal transduction studies. Their robust growth and established experimental protocols make them an ideal platform for creating gene knockouts to investigate molecular mechanisms in a cancer-relevant context.
CD47 functions primarily as an anti-phagocytic signal by engaging signal regulatory protein alpha (SIRP??) on macrophages, leading to activation of the tyrosine phosphatases SHP-1 (PTPN6) and SHP-2 (PTPN11), which inhibit phagocytic receptor signaling. Beyond immune evasion, CD47 interacts with thrombospondin-1 (THBS1) and integrin heterodimers including ??v??3 and ??IIb??3, modulating cell adhesion and migration through downstream effectors such as SRC and focal adhesion kinase (PTK2/FAK). Expression of CD47 is transcriptionally regulated by MYC, HIF1A, and NFKB1, linking it to oncogenic and inflammatory pathways.
In the HeLa cervical cancer model, CD47 knockout disrupts the “don’t eat me” signal, potentially enhancing the susceptibility of these cells to phagocytic clearance by macrophages in co-culture assays. This makes the CD47 knockout HeLa polyclonal population a powerful tool for dissecting immune evasion mechanisms in tumors and for validating therapeutic strategies targeting the CD47-SIRP?? axis. Moreover, because CD47 is involved in integrin-mediated adhesion, these cells enable investigation of how CD47 loss affects cell-extracellular matrix interactions and migratory behavior in cancer cells.
Researchers can employ this knockout model in a variety of experimental settings, including phagocytosis assays with primary or immortalized macrophages, flow cytometric confirmation of CD47 surface expression, Western blotting to assess total protein levels, and cell adhesion assays to evaluate integrin-dependent functions. Co-immunoprecipitation studies can further probe the interaction between CD47 and SIRP?? or other binding partners. These applications support studies in cancer immunotherapy target validation, phagocytosis signaling, and cell adhesion dynamics. For further information or technical assistance, please contact Ascent Research.
