The KLF4 Knockout DLD-1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the DLD-1 human colorectal adenocarcinoma cell line. This product provides a heterogeneous population of cells with targeted disruption of the KLF4 gene, enabling loss-of-function studies in a well-characterized colorectal cancer model. The polyclonal format preserves genetic diversity and is suitable for applications where clonal variation is desired or bulk functional screening is required.
DLD-1 is a widely used epithelial cell line established from a Dukes’ type C colorectal adenocarcinoma. These cells harbor mutations in key oncogenic pathways, including APC and KRAS, making them a relevant model for studying Wnt/??-catenin-driven tumorigenesis. The DLD-1 line exhibits robust in vitro growth, invasion capacity, and tumorigenicity in xenograft models, and is commonly employed for investigating colorectal cancer progression, metastasis, and drug responses.
KLF4 encodes a zinc-finger transcription factor that functions as a tumor suppressor in the colorectal epithelium. It is regulated by upstream signals such as TGF-??, p53, and ??-catenin/TCF, and transcriptionally activates downstream targets including CDKN1A (p21), CDH1 (E-cadherin), and BAX, while repressing CCND1 and BCL2. KLF4 interacts with co-regulators p300/CBP and HDACs, and forms complexes with POU5F1 (OCT4) and SOX2. In colorectal cancer, KLF4 antagonizes Wnt/??-catenin signaling by disrupting ??-catenin/TCF-mediated transcription and promoting differentiation. It also intersects with TGF-??/SMAD, MAPK/ERK, and PI3K/AKT pathways to control proliferation, apoptosis, and EMT.
In the context of DLD-1 cells, which exhibit constitutive Wnt pathway activation due to APC mutation, KLF4 knockout further elevates ??-catenin transcriptional activity and enhances tumorigenic properties. Loss of KLF4 in this background mimics aggressive colorectal cancer phenotypes, including increased proliferation, survival under stress, and invasive capacity. This model is therefore instrumental for dissecting the tumor-suppressive mechanisms of KLF4 and its interplay with oncogenic drivers. The polyclonal knockout population allows researchers to study the functional heterogeneity of KLF4 loss without clonal artifacts, making it valuable for screens and population-level analyses.
These polyclonal KLF4 knockout cells are suitable for a variety of assays, including western blotting, RT-qPCR, TOP/FOP luciferase reporter, and ChIP-qPCR. Functional assays can assess cell viability (MTT), apoptosis (Caspase-3/7), colony formation, and migration/invasion (Transwell). Applications include drug sensitivity profiling (IC50), EMT studies, and screening for pathway modulators in colorectal cancer. For further information, contact Ascent Research.
