The KDM1A Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HCT 116 cells with targeted disruption of the KDM1A gene. As a heterogeneous knockout pool, this product preserves genetic diversity while ensuring loss-of-function representation across the culture, making it ideal for studies where clonal uniformity is not required.
HCT 116 is a human colorectal carcinoma cell line commonly used in colon cancer research. It exhibits mismatch repair deficiency due to an MLH1 mutation, leading to microsatellite instability, and harbors an oncogenic KRAS G13D mutation that activates MAPK signaling. These cells are tumorigenic in vivo and widely applied in drug screening and mechanistic studies.
KDM1A (LSD1) is a histone demethylase that removes mono- and di-methyl marks from H3K4, functioning as a transcriptional corepressor. It acts within the CoREST complex with RCOR1, RCOR2, HDAC1, and HDAC2. KDM1A is regulated by upstream factors including HIF1A, MYC, REST, SNAI1, and TGFB1, and it represses tumor suppressors such as CDH1, CDKN1A, and PTEN, while influencing MYC and SNAI2 expression. Through these interactions, KDM1A promotes EMT and cell proliferation, intersecting with androgen receptor and Notch signaling.
In HCT 116 cells, KDM1A is often overexpressed and helps maintain malignancy by silencing tumor suppressor genes. Knockout of KDM1A in this context is expected to derepress CDH1 and CDKN1A, potentially restoring epithelial traits and impairing proliferation. The mismatch repair-deficient and KRAS-mutant background provides a relevant setting to investigate synthetic lethality and epigenetic dependencies in colorectal cancer, making this model valuable for preclinical LSD1 inhibitor evaluation.
Applications include ChIP-qPCR for H3K4me2 at target loci, western blotting for histone modifications, and RT-qPCR or RNA-seq for EMT marker expression. Proliferation, migration, and apoptosis assays can assess functional consequences. These cells are suited for LSD1 inhibitor validation and cancer stem cell research. For further details, please contact Ascent Research.
