The ABCF3 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ABCF3 gene in the HT29 human colorectal adenocarcinoma cell line. This polyclonal product provides a heterogeneous pool of cells carrying gene-disrupting edits, enabling functional studies without single-cell cloning. The mixed population maintains biological variability while ensuring efficient loss-of-function for reliable downstream assays.
HT29 is an adherent epithelial cell line derived from a 44-year-old Caucasian female with Duke??s stage B colorectal adenocarcinoma. It serves as a widely used model for intestinal epithelial biology and colorectal cancer, harboring key mutations in APC, TP53, and KRAS that mimic common driver events. These genetic alterations make HT29 cells particularly suitable for studying tumor progression, signal transduction, and drug responses.
ABCF3 is an ATP-binding cassette ATPase implicated in ribosomal biogenesis and translation regulation. It physically associates with ribosomal subunits and translation initiation factors such as eIF3 and eIF4F, acting as a facilitator of ribosome assembly and translation control. Although upstream signals remain unidentified, ABCF3-dependent disruption of translational machinery can alter expression of ribosomal proteins and translation factors, leading to widespread changes in protein synthesis.
In the HT29 colorectal cancer background, loss of ABCF3 disrupts translational control, providing a means to investigate how ribosomal dysfunction impacts cancer phenotypes. Because protein synthesis is critical for rapid proliferation and has been linked to drug resistance, this knockout model allows dissection of the role of ABCF3 in cell growth, survival, and chemosensitivity. The polyclonal design ensures that consistent biological effects are observed across an edited cell population.
These cells support diverse applications including analysis of translation regulation, drug resistance studies, and intestinal epithelial function assays. Standard methods such as western blotting, RT-qPCR, and immunofluorescence verify ABCF3 depletion and downstream effects on ribosomal proteins. Functional assays for proliferation, migration, invasion, and protein synthesis (e.g., puromycin incorporation) assess phenotypic outcomes, while drug sensitivity testing reveals altered responses to colorectal cancer chemotherapeutics. The cells are compatible with RNA-seq and ribosome profiling for global translational profiling. For further details, please contact Ascent Research.
