Description

The BSG Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human A549 lung adenocarcinoma epithelial cells, engineered to disrupt the BSG (CD147) gene. This loss-of-function model enables investigations into the multifaceted roles of BSG in tumor biology, extracellular matrix remodeling, and metabolic regulation without the confounding background expression of the endogenous protein. The cell line serves as a defined genetic background for dissecting BSG-dependent signaling networks and phenotypic outcomes in lung cancer research.

A549 cells were originally established from the lung adenocarcinoma tissue of a 58-year-old Caucasian male. These adherent epithelial cells exhibit characteristics of type II alveolar epithelial cells and represent a widely used model for studying lung adenocarcinoma biology, including tumorigenesis, invasion, metastasis, and drug response. The A549 host cell line retains key oncogenic mutations and signaling dependencies, making it a clinically relevant platform for functional genomics studies.

BSG, also known as CD147 or extracellular matrix metalloproteinase inducer (EMMPRIN), is a transmembrane glycoprotein that mediates matrix metalloproteinase (MMP) production, promotes extracellular matrix degradation, and facilitates tumor cell invasion. Its expression is regulated by upstream stimuli such as TGF-??, EGF, HIF-1??, and TNF-??. BSG functions as a chaperone for monocarboxylate transporters MCT1 and MCT4, thereby controlling lactate export and glycolytic flux. It also interacts with cyclophilin A to activate pro-inflammatory signaling cascades and associates with integrins and caveolin-1 to modulate cell adhesion and migration. Downstream, BSG signaling enhances expression of MMP-1, MMP-2, MMP-9, and VEGF, while engaging the PI3K/Akt and NF-??B pathways. Through these interactions, BSG coordinates a network linking metabolic adaptation, matrix degradation, and inflammatory responses.

In the A549 background, BSG is critically involved in lung adenocarcinoma progression by driving MMP-dependent invasion and metabolic reprogramming via MCT1/MCT4-mediated lactate transport. Disruption of BSG in this cell line is expected to impair these processes, providing a valuable tool for dissecting the contribution of BSG to the aggressive phenotype of lung cancer cells. The model is particularly relevant for investigating the interplay between glycolysis, extracellular matrix remodeling, and metastatic potential in non-small cell lung cancer.

Researchers can employ this knockout cell line in a variety of experimental assays, including MMP gelatin zymography to assess secreted protease activity, Matrigel invasion assays to evaluate metastatic capacity, and lactate transport assays to measure metabolic function. Co-immunoprecipitation and western blotting can be used to monitor BSG-interacting partners and downstream effector expression, while RT-qPCR and flow cytometry for CD147 surface expression enable validation of gene disruption. Xenograft tumor growth assays allow in vivo assessment of tumorigenic and metastatic potential. For further details regarding product specifications, customization, or bulk orders, please contact Ascent Research.