The HMG20B Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A-549 human lung adenocarcinoma cell line. This product features targeted disruption of the HMG20B gene, encoding the BRAF35 protein, a key component of the BRAF35-HDAC (BHC) transcriptional corepressor complex. The polyclonal format provides a mixed population of gene-edited cells, enabling robust functional studies without clonal selection effects. Researchers can use these cells to investigate loss-of-function phenotypes of HMG20B in a defined cancer model system.
The host cell line, A-549, is a widely used model of human lung adenocarcinoma originally derived from a 58-year-old male patient. These cells exhibit characteristic features of type II alveolar epithelial cells and harbor a KRAS G12S activating mutation alongside wild-type p53 status. This genetic background makes A-549 cells particularly suitable for studying oncogenic signaling and tumor biology, including chromatin remodeling and transcriptional control mechanisms in lung cancer.
HMG20B functions as a core subunit of the BHC complex, which mediates transcriptional repression through REST (RE1-silencing transcription factor). It interacts with LSD1 (KDM1A), HDAC1, HDAC2, CoREST (RCOR1), and BHC80 (PHF21A) to facilitate histone deacetylation and chromatin compaction at RE1 sites, thereby silencing neuronal genes such as BDNF and SCN2A in non-neuronal cells. Additionally, HMG20B has been implicated in mitotic progression and chromosome segregation, linking chromatin architecture to cell cycle control. The REST-HMG20B axis thus serves as a critical regulator of gene expression programs governing neurodevelopment and potentially tumor suppression.
In the A-549 lung adenocarcinoma context, loss of HMG20B allows dissection of REST complex function independent of neuronal differentiation. The presence of KRAS G12S and intact p53 provides a unique genetic environment to study how chromatin remodeling and transcriptional silencing contribute to cancer cell behavior, including proliferation, survival, and metastatic potential. This model enables investigation of whether HMG20B-dependent repression modulates oncogenic or tumor-suppressive pathways in lung epithelial cells.
Typical research applications include ChIP-qPCR to map REST complex occupancy at target loci, RT-qPCR or RNA-seq to assess derepression of RE1-controlled genes, and western blotting or co-immunoprecipitation to analyze protein interactions within the BHC complex. Functional assays such as immunofluorescence for mitotic markers, flow cytometric cell cycle analysis, and mitotic chromosome spread preparations can be employed to examine HMG20B??s role in mitosis. These polyclonal knockout cells are ideal for high-content screens investigating REST-mediated silencing or mitotic regulation in a cancer setting. For additional information, contact Ascent Research.
