The HMG20B Knockout NCI-H1975 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1975 human lung adenocarcinoma cell line, featuring targeted disruption of the HMG20B gene. This product provides a loss-of-function model suitable for investigating the functional role of HMG20B within chromatin regulatory complexes and its contribution to epigenetic gene silencing in a cancer context. The polyclonal format preserves population-level heterogeneity while enabling robust assessment of HMG20B-dependent phenotypes across a pool of edited cells.
The host cell line NCI-H1975 is a widely used human non-small cell lung cancer (NSCLC) model derived from a lung adenocarcinoma. Its genomic background includes activating EGFR mutations (L858R and T790M) and a TP53 mutation, which are representative of clinically relevant alterations driving tumor progression and drug resistance in EGFR-mutant NSCLC. These epithelial cells maintain key oncogenic signaling dependencies and are frequently employed in preclinical studies of EGFR-targeted therapies and epigenetic modulators.
HMG20B functions as a non-enzymatic component of the LSD1-CoREST histone demethylase complex and the neuron-specific BAF (nBAF) chromatin remodeling complex, contributing to transcriptional repression of neuronal genes through histone H3K4 demethylation. It interacts directly with LSD1 (KDM1A), CoREST (RCOR1), PHF21A, and BAF subunits such as SMARCC1 and SMARCA4. Upstream regulators include SOX2, OCT4, and PAX6, while downstream target genes repressed by this complex comprise SCN1A, STMN2, NEUROD1, and BDNF. Disruption of HMG20B abrogates complex integrity, potentially leading to derepression of these neuronal genes and concomitant alterations in chromatin states.
In the NCI-H1975 NSCLC background, knockout of HMG20B is expected to perturb LSD1-CoREST-mediated repressive functions, thereby relieving transcriptional silencing of neuronal gene programs that are normally inactive in lung epithelial cells. This aberrant expression may influence cancer cell behavior, including proliferation, differentiation, and sensitivity to epigenetic therapies. The model thus provides a valuable system to dissect the interplay between chromatin remodeling and oncogenic signaling in EGFR-mutant lung adenocarcinoma and to explore HMG20B as a contextual vulnerability.
This knockout polyclonal population is applicable to a range of research contexts, including functional interrogation of the LSD1-CoREST complex in lung cancer, mechanistic studies of ectopic neuronal gene expression in non-neuronal tumors, epigenetic target validation for LSD1 inhibitors, and chromatin remodeling investigations in EGFR-mutant NSCLC. Representative experiments include western blotting of HMG20B and its interactors, RT-qPCR analysis of STMN2 and SCN1A, ChIP-qPCR for H3K4me2 at target promoters, co-immunoprecipitation of LSD1-CoREST components, RNA-seq for transcriptomic profiling, and functional assays such as migration, invasion, cell viability, and apoptosis. For further information, please contact Ascent Research.
