The BCL7C Knockout A-549 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of A-549 cells with targeted disruption of BCL7C. This polyclonal knockout pool supports loss?of?function studies without single?clone isolation, providing a relevant model for population?based assays such as western blotting, transcriptomic analysis, and migration assays in a lung adenocarcinoma background.
The human A?549 cell line was established from the lung adenocarcinoma of a 58?year?old Caucasian male and exhibits characteristics of alveolar type II pneumocytes, including surfactant protein expression. It serves as a standard model for investigating lung cancer biology, epithelial?mesenchymal transition, and cell migration, with robust in vitro growth that facilitates reproducible genetic manipulation and experimental workflows.
BCL7C functions as a component of the SWI/SNF chromatin remodeling complex, interacting with SMARCA4, ARID1A, and SMARCB1 to regulate gene expression. It also associates with actin and profilin, linking to cytoskeletal dynamics and modulating ACTB and VIM. In the Wnt pathway, BCL7C acts downstream of WNT3A and WNT5A through ???catenin/TCF and regulates targets such as MMP2 and MMP9. TGF??? and Rho GTPase signals further impinge on BCL7C, placing it at the nexus of chromatin regulation, cytoskeletal organization, and apoptosis.
In A?549 cells, BCL7C deletion is relevant because SWI/SNF subunit mutations are prevalent in non?small cell lung cancer. This knockout model enables dissection of BCL7C??s tumor?suppressive roles, especially in controlling EMT and invasion. Loss of BCL7C may alter chromatin states affecting CDH1 and cytoskeletal remodeling, mimicking processes in metastatic progression. Combined with A?549 responsiveness to Wnt and TGF??? pathways, this system allows investigation of BCL7C loss in lung adenocarcinoma pathogenesis.
Applications include western blotting and RT?qPCR for knockdown validation, RNA?seq to map BCL7C?dependent transcriptomes, Transwell migration/invasion assays, immunofluorescence for actin organization, annexin V apoptosis assays, and ChIP for SWI/SNF?associated histone marks. Additional utility lies in drug sensitivity testing with HDAC and BET inhibitors. For further information, contact Ascent Research.
