The CD109 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting CD109 in the human HT29 colorectal adenocarcinoma cell line. Supplied as a heterogeneous pool of edited cells, this product provides a stable loss-of-function model for studying CD109-mediated regulatory mechanisms without the need for single-cell cloning. The CRISPR/Cas9-mediated gene disruption enables constitutive ablation of CD109 expression, suitable for functional studies requiring long-term knockout.
The HT29 host cell line, derived from a 44-year-old Caucasian female with colorectal adenocarcinoma, is an adherent, undifferentiated epithelial model with microvilli and expression of mucin and ion transporters. It displays absorptive and goblet-cell-like characteristics and harbors mutations in APC, TP53, and BRAF V600E, with microsatellite stability. Widely employed in cancer biology and intestinal barrier research, HT29 offers a clinically relevant context for investigating colorectal tumorigenesis.
CD109 is a GPI-anchored glycoprotein that negatively regulates TGF-?? signaling by functioning as a decoy receptor that binds TGF-?? ligands, limiting their availability for the TGFBR1-TGFBR2 complex. This suppression attenuates SMAD2/3 phosphorylation and downstream transcriptional responses, while also influencing non-canonical PI3K-AKT and MAPK/ERK pathways. CD109 is modulated by EGF, IL-6, STAT3, and hypoxia, and interacts with SARA and SMURF1; its loss can enhance expression of targets such as Cyclin D1 and MMP9, linking it to proliferation and invasion control.
In HT29 cells, CD109 knockout is anticipated to potentiate TGF-??-induced SMAD signaling, promoting invasive and metastatic phenotypes. The presence of BRAF V600E and TP53 mutations, which synergize with TGF-?? to drive EMT, heightens the relevance of this model. The polyclonal composition mirrors tumor heterogeneity, enabling studies of CD109 loss in a realistic cancer cell population context.
This knockout model enables TGF-?? signaling analysis via phospho-SMAD2/3 western blotting and reporter assays, gene expression profiling by RNA-seq/RT-qPCR, and functional assays such as Boyden chamber migration/invasion, proliferation, and apoptosis measurements. It is ideal for drug screening targeting TGF-?? pathway inhibitors and for co-immunoprecipitation studies of altered protein interactions. For further information, please contact Ascent Research.
