The ELAVL1 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with disrupted ELAVL1 in HCT 116 cells. This polyclonal pool provides a heterogeneous loss-of-function model ideal for population-level studies of ELAVL1 (HuR)-dependent post-transcriptional regulation. The product is generated via CRISPR/Cas9-mediated gene disruption, avoiding clonal selection biases and offering a robust tool for functional genomics.
HCT 116 is a human colorectal adenocarcinoma cell line deficient in MLH1, resulting in high microsatellite instability (MSI-H). It is a widely employed model for studying colorectal cancer, particularly MSI-H tumors and DNA mismatch repair defects, and is valued for its well-characterized signaling pathways and robust tumorigenic growth in vitro and in vivo.
ELAVL1 binds AU-rich elements (AREs) in 3?? UTRs, stabilizing target mRNAs such as Cyclin D1, Bcl-2, c-Myc, VEGFA, PTGS2, and CDKN1A. Its activity is regulated by p38 MAPK, Chk2, PKC, SIRT1, and stresses like TNF-?? and oxidative stress. ELAVL1 interacts with ANP32A, hnRNP A2/B1, TTP (ZFP36), importins/exportins, and miRNAs miR-519 and let-7. It integrates p53, MAPK/ERK, and Wnt/??-catenin pathways, linking p53 to p21 stabilization, MAPK to ELK1, and Wnt/??-catenin/TCF to Cyclin D1 expression, thereby controlling proliferation, survival, and stress responses.
In the context of HCT 116 MLH1 deficiency and MSI-H, ELAVL1 knockout severely attenuates the post-transcriptional stabilization of key oncogenic and survival transcripts, including Cyclin D1 and Bcl-2. This leads to diminished cell proliferation, increased apoptosis, and reduced tumorigenic potential, making the model essential for examining how RNA stability mechanisms interact with DNA repair defects to promote aggressive colorectal cancer.
This polyclonal knockout product supports research in cancer biology, post-transcriptional gene regulation, drug resistance, metastatic progression, and apoptosis. Representative assays include RNA immunoprecipitation, CLIP-seq, RNA-seq, RT-qPCR, Western blotting, MTT/BrdU proliferation, Annexin V apoptosis, Transwell migration/invasion, ARE-luciferase reporters, and drug sensitivity screening. These cells enable comprehensive dissection of ELAVL1-dependent networks for target and biomarker discovery. For further information, please contact Ascent Research.
