The KIF16B Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the HT29 human colorectal adenocarcinoma cell line with targeted disruption of KIF16B. This loss-of-function model enables detailed investigation of microtubule-dependent early endosome transport in epithelial cancer research. The polyclonal format captures diverse editing events, providing a physiologically relevant system to examine how KIF16B deficiency impacts cellular processes.
The HT29 parental cell line originates from a human female colorectal adenocarcinoma and is widely employed as a model for intestinal epithelial differentiation and barrier function. These adherent cells retain tumorigenic features and can be induced to differentiate, making them a robust platform for studying colorectal cancer biology, particularly mechanisms governing cell polarity, migration, and drug sensitivity.
KIF16B is a plus-end-directed kinesin-3 motor that drives microtubule-based transport of early endosomes. It interacts with dynamin-2, Rab5, Rab4, dynein, and sorting nexin 4 (SNX4), and is recruited to PI(3)P-rich membranes. Acting downstream of EGFR signaling and PI3K activation, KIF16B controls the recycling versus degradation fate of internalized receptors such as EGFR. Knockout of KIF16B disrupts endosomal sorting, leading to altered EGFR stability and downstream ERK phosphorylation, as well as dysregulated mTOR signaling, ultimately affecting cell proliferation and migration.
In the context of HT29 colorectal adenocarcinoma cells, KIF16B knockout provides a valuable system to dissect how endosomal dynamics intersect with oncogenic signaling pathways. HT29 cells depend on proper EGFR trafficking for sustained growth and motility signals. By perturbing KIF16B-dependent endosome transport, researchers can explore how mislocalization of receptor tyrosine kinases contributes to colorectal cancer phenotypes.
This polyclonal knockout model supports diverse applications, including studies on colorectal cancer metastasis, endocytosis, drug resistance, and cell migration. Relevant assays include Western blotting for EGFR and phospho-ERK, fluorescent transferrin uptake, transwell migration/invasion, immunofluorescence for EEA1 and Rab5, and MTT proliferation. CRISPR-mediated gene disruption can be verified by sequencing. For additional information, please contact Ascent Research.
