CD44 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HeLa cells, offering a loss-of-function model for the hyaluronan receptor CD44. The polyclonal format provides a heterogeneous knockout pool to study CD44-dependent processes while avoiding clonal artifacts. This product is designed for investigating the molecular and cellular roles of CD44 in a cervical epithelial adenocarcinoma context.
HeLa is an HPV18-positive cervical adenocarcinoma cell line, widely used as a model for cervical cancer and epithelial biology. Its transformed phenotype and well-characterized signaling networks make it a robust platform for examining genes involved in tumor progression and metastasis. The immortalized nature of HeLa cells supports reproducible gene editing and functional assays.
CD44 is the principal hyaluronan receptor, mediating cell adhesion and signal transduction. Upon hyaluronan binding, CD44 activates the PI3K/AKT and MAPK/ERK cascades, promoting proliferation, survival, and migration. It couples the extracellular matrix to the actin cytoskeleton via ERM proteins (ezrin, radixin, moesin) and is regulated by upstream stimuli including TNF-??, IL-1??, EGF, TGF-??, and Wnt ligands through ??-catenin/TCF. Downstream targets encompass ERK1/2, AKT, NF-??B, RhoA, Rac1, and transcriptional upregulation of MMP9, cyclin D1, and c-Myc. Interacting factors such as hyaluronan, ezrin, osteopontin, and MMP14 modulate CD44 function. The receptor??s signaling network includes key components like hyaluronan, CD44, ezrin, Src, Ras, PI3K, AKT, ERK, and NF-??B.
In HeLa cells, CD44 is often overexpressed and contributes to a metastatic phenotype by enhancing adhesion to hyaluronan-rich matrices and activating pro-survival pathways. This polyclonal knockout model enables rigorous dissection of CD44??s role in cervical cancer progression, including its effects on PI3K/AKT and MAPK/ERK pathway activation, NF-??B transcriptional programs, and Rho GTPase-driven cytoskeletal dynamics. Researchers can assess how loss of CD44 impacts cell adhesion, migration, invasion, and drug sensitivity in a relevant epithelial cancer background.
Research applications include transwell migration and invasion assays to quantify metastatic potential, hyaluronan binding assays to measure receptor-ligand interaction, and western blot analysis for CD44, phospho-AKT, and phospho-ERK. Flow cytometry verifies knockout efficiency by assessing CD44 surface expression. Tumor spheroid formation assays enable 3D growth studies, while drug response assays probe CD44-mediated chemoresistance. These tools support mechanistic studies and therapeutic target validation in cervical cancer. For further technical inquiries, please contact Ascent Research.
