The ADNP2 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the ADNP2 gene, enabling functional studies of ADNP2 in a colorectal cancer context. The polyclonal format preserves cellular diversity and mitigates clonal artifacts, making it suitable for phenotypic screening and population-level assays. The knockout model serves as a loss-of-function tool to dissect ADNP2’s role in transcriptional regulation and chromatin remodeling.
The HT29 parental cell line is a well-established model of human colorectal adenocarcinoma with epithelial morphology. Originally isolated from a primary tumor, HT29 cells are widely used in cancer research to study intestinal epithelial biology, tumor progression, and therapeutic responses. They exhibit characteristic features of colorectal cancer, including aberrant Wnt signaling and the capacity for differentiation under specific conditions. This background provides a disease-relevant context for investigating ADNP2’s functions in colorectal tumorigenesis.
ADNP2 encodes a zinc finger homeobox protein that operates as a chromatin-associated transcription factor. It integrates with SWI/SNF chromatin remodeling complexes, interacting with core components such as BRG1 and BAF170, and further associates with heterochromatin protein 1 alpha (HP1??) and histone deacetylases. ADNP2 functions as a scaffold that links upstream transcription factors??including SP1, E2F family members, and putative Wnt-responsive factors??to chromatin modification, thereby modulating the expression of downstream targets like CCND1, MYC, and BCL2. Through these interactions, ADNP2 regulates gene programs governing cell proliferation, survival, and differentiation.
In the context of HT29 colorectal cancer cells, ADNP2 knockout provides a powerful model to examine the intersection of chromatin remodeling and oncogenic transcription. Given the frequent dysregulation of SWI/SNF components and Wnt/??-catenin signaling in colorectal cancer, ADNP2 loss may reveal how chromatin-level control contributes to tumor cell proliferation, apoptosis evasion, and metastatic potential. This polyclonal knockout population allows researchers to assess the average effect of ADNP2 disruption without clonal bias, reflecting the heterogeneous nature of tumors.
Researchers can employ this product in a wide range of applications, including functional characterization of ADNP2 in colorectal cancer proliferation using MTT and colony formation assays, migration/invasion studies via Transwell assays, and gene expression analysis by RT-qPCR and RNA-seq. Chromatin immunoprecipitation (ChIP) with antibodies against SWI/SNF components like BRG1 can probe altered complex binding at key loci. Additionally, drug target discovery and synthetic lethality screens benefit from this model. For further details or to request this product, please contact Ascent Research.
