The ICAM1 Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of human 143B osteosarcoma cells with targeted disruption of the ICAM1 gene. This loss-of-function model provides a heterogeneous pool of edited alleles, enabling the study of ICAM1-dependent functions without clonal selection. The knockout eliminates ICAM1 surface expression, impairing key adhesion and migration processes mediated by this immunoglobulin superfamily member.
The 143B cell line is a well-characterized adherent, fibroblast-like osteosarcoma line originally established from a human bone tumor. As a mesenchymal tumor model, 143B cells exhibit high metastatic potential, particularly to lung and bone, making them a relevant system for investigating mechanisms of cancer dissemination. Their robust growth and genetic tractability facilitate CRISPR-based engineering and downstream functional assays.
ICAM1 encodes intercellular adhesion molecule 1 (CD54), a transmembrane glycoprotein that serves as a counter-receptor for the leukocyte integrins LFA-1 (??L??2, CD11a/CD18) and Mac-1 (??M??2, CD11b/CD18). Binding to these integrins mediates firm adhesion and crawling of leukocytes on endothelial surfaces, a critical step in transendothelial migration. ICAM1 expression is upregulated by inflammatory cytokines, including TNF-??, IL-1??, and IFN-??, acting through NF-??B and AP-1 transcription factors. Downstream, ICAM1 engagement triggers intracellular signaling via ERM proteins (ezrin, radixin, moesin), RhoA, and ROCK, regulating cytoskeletal reorganization. It also interacts with fibrinogen, hyaluronan, and can be exploited as a receptor by filoviruses. In endothelial and immune contexts, ICAM1 collaborates with VCAM1, PECAM1, JAM-A, and ESAM to orchestrate leukocyte diapedesis.
In 143B osteosarcoma cells, ICAM1 knockout disrupts both homotypic tumor cell adhesion and heterotypic interactions with leukocytes, potentially impairing the metastatic cascade. Given the mesenchymal origin and metastatic propensity of 143B, loss of ICAM1 may reduce tumor cell extravasation and colonization at secondary sites. The knockout model also permits analysis of how tumor-derived ICAM1 influences the immune microenvironment, as ICAM1-mediated adhesion can modulate natural killer cell and T-cell responses. Furthermore, because osteosarcoma metastasizes to bone, a tissue rich in ICAM1 ligands, this model is instrumental for dissecting adhesion-dependent bone tropism.
This polyclonal knockout cell product is designed for a broad array of research applications, including static and dynamic adhesion assays with labeled leukocytes, Transwell migration and invasion studies, and co-culture experiments to assess immune cell infiltration. Flow cytometry and Western blotting can verify loss of ICAM1 protein, while transcriptomic profiling (RNA-seq) reveals global expression changes. In vivo metastasis models, such as tail vein injection in immunocompromised mice, can evaluate the role of tumor ICAM1 in organ colonization. These cells are also suitable for drug target validation, testing anti-adhesion therapies, and studying the interplay between inflammation and cancer progression. For additional technical information, please contact Ascent Research.
