MCAM Knockout Raji Polyclonal Cells are a human B lymphocyte polyclonal knockout cell population derived from the Raji cell line, generated via CRISPR/Cas9-mediated disruption of the MCAM gene. This polyclonal knockout model provides a heterogeneous pool of cells with MCAM gene ablation, enabling robust loss-of-function studies in a lymphoma background. It is suitable for investigating MCAM’s role in cell adhesion, signaling, and tumor biology.
Raji is an EBV-positive B lymphoblastoid cell line established from a Burkitt lymphoma patient. Widely used in immunology and lymphoma research, Raji cells exhibit malignant B cell characteristics, including rapid proliferation and expression of B cell surface markers. The cell line serves as a well-characterized model for studying B cell receptor signaling, oncogenic pathways, and immune cell interactions. Its derivation from an aggressive lymphoma makes it particularly relevant for investigating tumor cell adhesion, survival, and metastasis.
MCAM (CD146) is a cell adhesion molecule mediating homophilic cell-cell adhesion and is implicated in lymphocyte transmigration, angiogenesis, and tumor progression. In the context of Raji cells, MCAM interacts with actin filaments, ezrin, ??-catenin, and integrin ??4??1 to regulate adhesion and cytoskeletal dynamics. Mechanistically, MCAM signaling converges on the PI3K/AKT and NF-??B pathways. Upon ligand engagement, MCAM activates the PI3K/AKT axis, leading to phosphorylation of AKT and downstream modulation of Cyclin D1, contributing to proliferation and survival. Additionally, MCAM stimulates the NF-??B pathway via the IKK complex, promoting nuclear translocation of NF-??B p65 and transcriptional upregulation of target genes such as MMP-2, MMP-9, and VEGF, which facilitate invasion and angiogenesis. The transcription factors NF-??B and AP-1, along with cytokines TNF-?? and IL-1??, act as upstream regulators inducing MCAM expression, forming a positive feedback loop. STAT3 also participates in MCAM signaling, further linking to cell growth and immune evasion.
Disruption of MCAM in Raji B lymphoma cells abrogates MCAM-mediated cell adhesion and attenuates downstream PI3K/AKT and NF-??B signaling. This loss-of-function model results in reduced proliferation, survival, and invasive capacity, mirroring the functional consequences of MCAM inhibition in lymphoid malignancies. The polyclonal population allows assessment of heterogeneous responses to MCAM knockout, reflecting the genetic diversity within tumor cell populations. It enables dissection of MCAM??s role in B cell lymphoma pathogenesis, including its involvement in interactions with the tumor microenvironment and transendothelial migration. Furthermore, the model provides a platform for evaluating the impact of MCAM loss on drug sensitivity, given the contribution of PI3K/AKT and NF-??B pathways to chemoresistance.
Researchers can employ these MCAM Knockout Raji Polyclonal Cells for a wide range of functional studies. Typical applications include cell adhesion and migration assays using Transwell systems, flow cytometric analysis of adhesion molecules, immunofluorescence staining for subcellular localization, and Western blotting for phospho-AKT and other signaling proteins. RT-qPCR can be used to validate downstream target expression such as MMP-9 and VEGF. Apoptosis assays and drug sensitivity profiling can assess the loss of MCAM on cell death and therapeutic response. These cells are also valuable for investigating the crosstalk between MCAM and integrin-mediated adhesion or for studying the role of MCAM in immune cell trafficking in the context of inflammatory diseases like rheumatoid arthritis and atherosclerosis. For further information, please contact Ascent Research.
