The HABP4 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line HT29. This product provides a loss-of-function model for investigating the biological roles of HABP4, an RNA-binding protein involved in stress granule formation and mRNA metabolism. The polyclonal format preserves the genetic heterogeneity of the parental cell population while enabling robust analysis of gene function following targeted disruption. This approach is well-suited for studies examining population-level responses to gene knockout without the clonal selection biases inherent in single-cell-derived lines.
HT29 cells are a widely characterized human colorectal adenocarcinoma epithelial line that serves as a model for colonic epithelial barrier function, ion transport, and enterocytic differentiation. These cells retain the capacity to differentiate into mucus-secreting goblet-like cells under appropriate culture conditions and express markers typical of intestinal epithelium. Their tumorigenic origin and well-documented signaling pathways make them a valuable platform for dissecting colorectal cancer biology, drug responsiveness, and the mechanistic basis of epithelial homeostasis.
HABP4, also known as a hyaluronan-binding protein, functions as a multifunctional RNA-binding protein that integrates hyaluronan signaling with post-transcriptional gene regulation. It participates in the assembly of stress granules and processing of mRNAs, and it is activated by phosphorylation through protein kinase C (PKC) and checkpoint kinase 1 (CHEK1). HABP4 interacts with partners such as p53, TOPORS, RACK1, and stress granule core components G3BP1 and TIA-1. This protein acts downstream of hyaluronan and cellular stress cues, transcriptionally regulating a subset of p53 target genes and modulating the fate of stress granule-associated mRNAs. Its molecular network bridges extracellular matrix signals, the DNA damage response, and the control of mRNA stability under stress conditions.
In the context of HT29 colorectal cancer cells, disruption of HABP4 is expected to alter the cellular response to oxidative stress, heat shock, and chemotherapeutic agents. Because HABP4 links hyaluronan??a major tumor microenvironment component??with p53-dependent transcriptional programs, its knockout may impair stress granule dynamics, modify cell proliferation, and affect sensitivity to treatments that activate the p53 pathway. This model therefore enables dissection of how HABP4 influences colorectal cancer cell plasticity, survival signaling, and the interplay between environmental cues and gene expression.
Typical research applications include investigations into stress granule biology, mRNA regulation in cancer, p53 signaling modulation, and drug resistance mechanisms. Researchers can employ this knockout model to perform western blotting for HABP4, RT-qPCR of stress markers, immunofluorescence of stress granule proteins, cell viability and migration assays, phospho-signaling analysis of PKC and CHEK1, RNA-seq transcriptomic profiling, and co-immunoprecipitation of HABP4 complexes. These approaches facilitate the study of colorectal cancer cell signaling and the identification of therapeutic vulnerabilities. For further information, please contact Ascent Research.
