The HMGN3 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line HT29, with targeted disruption of the high mobility group nucleosome-binding protein 3 (HMGN3) gene. This product provides a heterogeneous knockout model for loss-of-function studies, enabling researchers to interrogate HMGN3-dependent chromatin regulation and transcriptional control in a colorectal cancer context.
The HT29 cell line originates from a primary adenocarcinoma of the colon in a 44-year-old female and exhibits epithelial morphology with the capacity to form tight junctions and produce mucins. As a well-established model for intestinal epithelial biology and disease, HT29 cells are extensively employed to study colorectal cancer pathophysiology, epithelial barrier function, and signaling mechanisms underlying tumor progression.
HMGN3 is a chromatin architectural protein that binds directly to nucleosomes, modulating chromatin structure and accessibility to regulate transcription. In the Wnt/??-catenin signaling pathway, HMGN3 functions downstream of Wnt3a, ??-catenin (CTNNB1), and TCF4/LEF1, and is also regulated by EGF. It interacts with nucleosomes, histone H1, the SWI/SNF chromatin remodeling complex, and TCF4. HMGN3 transcriptionally promotes the expression of key metabolic targets including SLC2A1 (GLUT1), HK2, and PFKL, as well as the cell cycle regulator CCND1, thereby linking chromatin dynamics to glycolytic gene programs and proliferation.
Knockout of HMGN3 in HT29 cells eliminates its nucleosome-binding function, leading to altered chromatin accessibility at Wnt-responsive loci and reduced expression of SLC2A1 and other downstream targets. This disruption impairs glucose uptake and glycolytic flux, attenuates cell proliferation, and highlights the role of HMGN3 in sustaining the metabolic reprogramming characteristic of the Warburg effect in colorectal cancer cells. The polyclonal nature of the population maintains heterogeneous editing outcomes, offering a robust model for studying gene function without clonal selection bias.
This knockout model is suited for a range of colorectal cancer research applications, including investigation of chromatin-mediated gene regulation, metabolic rewiring, and Wnt pathway dynamics. It supports assays such as western blotting, RT-qPCR, ChIP-qPCR, glucose uptake measurement with 2-NBDG, MTT and colony formation assays, RNA-seq, and flow cytometric cell cycle analysis, facilitating detailed mechanistic and phenotypic studies. For further information, please contact Ascent Research.
