BSG Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population harboring targeted disruption of the BSG gene, which encodes the transmembrane glycoprotein Basigin (CD147/EMMPRIN). This loss-of-function model provides a reproducible and genetically stable system for investigating Basigin-mediated cellular processes without the limitations of transient silencing methods. The polyclonal knockout format ensures population-level representation of gene disruption while maintaining the intrinsic characteristics of the HAP1 host cell line.
The host cell line HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line, retaining the BCR-ABL1 oncogenic fusion characteristic of CML. HAP1 cells are adherent and near-haploid, with a diploid chromosome 8, making them particularly amenable to genetic manipulation and functional genomics studies. This genetic simplicity, combined with the oncogenic background, establishes HAP1 as a robust model for dissecting pathways relevant to leukemia and solid tumor biology.
Basigin is a multifunctional transmembrane glycoprotein that functions as an MMP inducer, a receptor for cyclophilin A and Plasmodium falciparum PfRh5, and a chaperone for MCT1 and MCT4. Through interactions with integrins ??3??1 and ??6??1, caveolin-1, and cyclophilins, it activates PI3K/Akt, MAPK/ERK, NF-??B, and Wnt/??-catenin signaling. Upstream regulators TNF-??, IL-1??, TGF-??, EGF, and HIF-1??, together with transcription factors Sp1 and AP-1, induce BSG expression. Downstream, Basigin promotes MMP-1, MMP-2, MMP-9, and MMP-14 expression, facilitating extracellular matrix remodeling and invasion. Additionally, Basigin chaperones MCT1 and MCT4, regulating lactate transport and glycolysis. BSG knockout therefore disrupts both MMP-mediated invasion and MCT-dependent metabolism.
In the HAP1 leukemic background, BSG knockout disrupts key oncogenic and metabolic axes. Basigin??s interaction with MCTs is critical for lactate shuttling, and its loss can impair glycolytic flux, potentially sensitizing these BCR-ABL1-driven cells to metabolic stress. Furthermore, the attenuation of MMP induction reduces invasive capacity, which is relevant for studies of leukemia dissemination and the metastatic behavior of solid tumors. The model thus enables dissection of Basigin-dependent pathways that co-operate with BCR-ABL1 signaling, including PI3K/Akt and MAPK/ERK cascades, and may inform on mechanisms of therapy resistance.
This BSG knockout model is ideally suited for a broad range of applications, including mechanistic studies of cancer invasion and metastasis, MMP regulation, anti-malarial drug screening targeting PfRh5?CBasigin interactions, and metabolic reprogramming research focused on MCT-dependent lactate transport. It also serves as a valuable tool for investigating immune synapse formation, inflammatory signaling, and drug resistance mechanisms. Representative assays that leverage this model include Western blotting, RT-qPCR, migration and invasion assays, gelatin zymography for MMP activity, immunofluorescence, flow cytometry, co-immunoprecipitation of Basigin interactors, lactate transport measurements, and cell viability/apoptosis assays. For further information, please contact Ascent Research.
