BCAM Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the BCAM (basal cell adhesion molecule) gene is disrupted, generating a loss-of-function model for investigating BCAM-dependent cellular processes. This product consists of a heterogeneous pool of edited HeLa cells, reflecting the natural diversity of CRISPR/Cas9-mediated gene disruptions without clonal selection, and is suitable for functional studies where polyclonal representation minimizes off-target clonal artifacts.
The host HeLa cell line is an immortalized human epithelial cell line originally derived from a cervical adenocarcinoma, positive for human papillomavirus 18 (HPV-18). Widely employed as a cervical cancer model, HeLa cells provide a robust and extensively characterized platform for studying tumor biology, signal transduction, and cell adhesion mechanisms, making them a relevant context for examining BCAM function.
BCAM encodes a laminin receptor that mediates cell attachment to laminin-511 and laminin-521, initiating focal adhesion assembly and downstream signaling cascades. Upon laminin binding, BCAM associates with integrin ??3??1 and CD44, leading to recruitment and phosphorylation of focal adhesion kinase (FAK) and Src kinase. These proximal events propagate signals through ERK1/2 and Akt pathways, thereby regulating actin cytoskeleton dynamics via RhoA and Rac1. BCAM expression is modulated by upstream regulators TGF-??1 and TNF-??, positioning BCAM as a key integrator of extracellular matrix signals with intracellular pathways governing cell migration, proliferation, and survival.
In the HeLa cervical cancer context, BCAM-mediated laminin adhesion is implicated in tumor cell migration and invasion. Disruption of BCAM in these polyclonal knockout cells abrogates laminin-induced focal adhesion formation and attenuates the FAK-Src-ERK/Akt signaling axis, providing a direct model to dissect the contribution of BCAM to oncogenic signaling. This model is particularly suited to studying how loss of BCAM impacts metastatic potential and responsiveness to microenvironmental cues.
These BCAM knockout HeLa polyclonal cells are applicable to a wide range of experimental approaches, including laminin adhesion assays, Transwell migration, wound healing, and immunofluorescence staining for focal adhesion components. Western blotting and phospho-specific ELISA can be used to quantify changes in FAK, ERK1/2, and Akt phosphorylation, while flow cytometry enables confirmation of BCAM surface loss. Potential applications extend to screens for anti-metastatic compounds and investigations of sickle cell adhesion mechanisms. For further product information or technical inquiries, please contact Ascent Research.
