The ELAVL2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population designed for loss-of-function analysis of the ELAVL2 gene. Generated by disrupting ELAVL2 in HT29 cells, this heterogeneous pool of edited alleles ablates gene function and retains population diversity, making it suitable for studies that benefit from genetic heterogeneity. This model provides a robust tool to investigate ELAVL2-mediated post-transcriptional regulation without requiring clonal isolation.
HT29 is a human colorectal adenocarcinoma cell line with epithelial morphology, isolated from a primary tumor and widely used in cancer research. These cells serve as a model for intestinal epithelial biology, colorectal tumorigenesis, and drug screening. Characterized by mutations in APC, TP53, and KRAS, HT29 provides a relevant genetic context for studying oncogenic signaling. The adherent line retains some differentiated features, including tight junction formation and mucin production, making it valuable for dissecting epithelial-specific processes.
ELAVL2 encodes an RNA-binding protein that stabilizes and regulates translation of target mRNAs via AU-rich elements (AREs) in their 3?? UTR. In neuronal cells, its activity is regulated by neuronal activity, neurotrophic factors, and cAMP signaling. ELAVL2 directly binds GAP43 and tau mRNAs, enhancing their expression. It interacts with HuR (ELAVL1), RNA polymerase II, and exon junction complex components to form post-transcriptional regulatory complexes. This protein integrates extracellular cues with gene expression output, primarily controlling transcript stability and ribosomal engagement. Although best characterized in neurons, ELAVL2 may influence mRNA metabolism in other cell types, providing a rationale for investigation in colorectal cancer.
Disruption of ELAVL2 in HT29 cells enables dissection of post-transcriptional regulatory mechanisms in colorectal cancer. As a modulator of mRNA stability, ELAVL2 may influence transcripts involved in proliferation, differentiation, and migration. Its loss in this epithelial adenocarcinoma model can reveal how ARE-mediated control contributes to tumorigenic phenotypes. This knockout system is well-suited for evaluating the functional consequences of ELAVL2 deficiency on cell behavior, including anchorage-independent growth, invasion, and drug response, thereby exposing vulnerabilities in the post-transcriptional network.
Typical applications include studying post-transcriptional regulation in colorectal cancer, investigating ELAVL2??s role in epithelial differentiation, functional genomics, and drug target validation. These cells are compatible with Western blotting, RT-qPCR, RNA-seq, immunofluorescence, migration/invasion, proliferation, and dual-luciferase reporter assays. The polyclonal population supports experiments requiring genetic diversity, such as drug selection or tumor evolution modeling. This product serves as a versatile platform for interrogating RNA-binding protein function in a malignant epithelial context. For additional information, contact Ascent Research.
