The ARMC9 Knockout HT29 Polyclonal Cells are a polyclonal CRISPR/Cas9-edited population of HT29 human colorectal adenocarcinoma cells carrying targeted disruption of the ARMC9 gene. The heterogeneous pool of edited alleles enables robust population-level functional studies without clonal bias. This loss-of-function model supports advanced research into ARMC9-dependent processes.
The HT29 host cell line is a well-characterized epithelial colorectal adenocarcinoma model with inactivating mutations in APC and TP53 and microsatellite stability (MSS). HT29 cells are widely used to study colorectal cancer biology and retain the capacity for enterocytic differentiation, making them suitable for examining ciliary and signaling dynamics in an intestinal malignancy context.
ARMC9 encodes a centrosome- and cilium-localized armadillo repeat protein essential for primary cilium assembly and Hedgehog (Hh) signal transduction. It interacts with ciliary transition zone components CEP41, CCDC66, INPP5E, and CEP290 to facilitate ciliogenesis and propagate Hh signaling from SHH through PTCH1, SMO, and SUFU to the GLI1/2/3 transcription factors. ARMC9 expression is driven by RFX3 and FOXJ1, and its disruption impairs GLI-dependent transcription, attenuating the Hh pathway and its crosstalk with Wnt signaling.
In HT29 cells, ARMC9 knockout permits dissection of primary cilia and Hh signaling contributions to colorectal cancer biology. This model is relevant for understanding how ciliary dysfunction intersects with APC/TP53 mutations and for studying context-dependent roles in proliferation, differentiation, and drug sensitivity. Moreover, the model aids ciliopathy research, including Joubert syndrome 30, by enabling analysis of ARMC9 function in a genetically tractable human epithelial background.
Researchers can employ this polyclonal knockout for immunofluorescence of ciliary markers (acetylated tubulin, ARL13B), Gli-dependent luciferase reporter assays, western blot of GLI1 processing, MTS proliferation and scratch wound migration assays, RNA-seq for pathway enrichment, and drug sensitivity testing with Hh inhibitors like vismodegib. Applications span functional dissection of cilia-dependent signaling, Hedgehog modulator screening, and ciliopathy modeling. For further information, please contact Ascent Research.
