The JDP2 Knouckout HT29 Polyclonal Cells provide a CRISPR/Cas9-mediated gene-disrupted polyclonal population for investigating the tumor-suppressive role of JDP2 in colorectal cancer. Derived from the HT29 cell line, these cells contain a heterogeneous mix of JDP2 knockout alleles generated by CRISPR/Cas9 editing, offering a loss-of-function model that preserves polyclonal diversity. This format is particularly advantageous for assays requiring robust bulk measurements, as it minimizes clonal artifacts and better represents the genetic heterogeneity of tumor cell populations.
The HT29 cell line originates from a human colorectal adenocarcinoma and exhibits epithelial morphology. These cells are capable of enterocytic differentiation upon induction with agents such as butyrate or glucose deprivation, making them a widely used in vitro system for studying intestinal epithelial biology, including transport processes, barrier integrity, and differentiation pathways. Their well-established tumorigenic features and responsiveness to genetic manipulation further establish them as a central model in colorectal cancer research.
JDP2 functions as a transcriptional repressor that antagonizes AP-1 activator complexes by binding to TRE/CRE sequences and recruiting HDAC1 and HDAC3 to chromatin. This repression modulates expression of key cell-cycle and invasion regulators such as cyclin D1 (CCND1), matrix metalloproteinases (MMP1 and MMP3), c-Myc, and the cyclin-dependent kinase inhibitor p21 (CDKN1A). JDP2 activity is regulated by upstream mitogenic stimuli, growth factors (EGF, FGF), pro-inflammatory cytokines (IL-6), and cellular stress signals (oxidative stress, UV light), linking it to the JNK/MAPK and p53/p21 pathways. In colorectal cancer, loss of JDP2 derepresses AP-1 target genes, contributing to enhanced proliferation and metastatic potential.
Within the HT29 model, JDP2 knockout disinhibits AP-1-mediated transcription, leading to increased cell cycle progression, migratory capacity, and invasive behavior, as well as alterations in apoptotic responses. This polyclonal knockout system enables the dissection of JDP2-dependent molecular mechanisms in a context that mirrors intratumoral heterogeneity, facilitating the identification of robust phenotypic changes and the evaluation of therapeutic agents targeting AP-1-driven oncogenic programs.
These cells support a wide range of functional analyses, including AP-1 luciferase reporter assays, cell proliferation measurements via MTT or BrdU, transwell migration and invasion tests, flow-cytometric cell cycle and apoptosis (Annexin V) assessments, and co-immunoprecipitation of JDP2 with c-Jun or HDAC complexes. Transcriptomic approaches such as RNA-seq can identify genome-wide JDP2-dependent gene signatures. For technical support or product inquiries, please contact Ascent Research.
