The CD44 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CD44 gene in the human HGC-27 gastric adenocarcinoma cell line. This product provides a heterogeneous pool of edited cells, enabling loss-of-function studies without clonal selection artifacts. The polyclonal format captures the variability inherent in gene editing, supporting robust functional analyses across diverse genetic backgrounds. CRISPR/Cas9-mediated target-gene disruption has been employed to abolish CD44 expression, creating a valuable model for investigating CD44-dependent biological processes in a metastatic gastric cancer context.
The HGC-27 host cell line is an epithelial cell line originally derived from the lymph node metastasis of a human gastric carcinoma. Characterized by its epithelial morphology, HGC-27 is widely utilized in gastric cancer research, particularly for studying metastatic mechanisms. The metastatic origin of this line makes it an appropriate model for examining the molecular determinants of tumor dissemination. The knockout of CD44 in these cells allows precise dissection of the receptor??s contribution to the aggressive behavior of gastric cancer, including adhesion, migration, and invasion, within a well-established experimental system.
CD44 is a transmembrane glycoprotein that serves as a primary receptor for hyaluronan and other extracellular matrix components such as osteopontin. Upon ligand binding, CD44 activates intracellular signaling through interactions with Src family kinases and adaptor proteins like ezrin, leading to stimulation of the PI3K/AKT and MAPK/ERK pathways. These cascades modulate downstream targets including MMP-9, VEGF, cyclin D1, and Rho GTPases, thereby promoting cell proliferation, survival, and motility. Expression of CD44 is transcriptionally regulated by WNT/??-catenin, NF-??B, and AP-1, integrating signals from oncogenic and inflammatory stimuli. This network underscores CD44??s role in hyaluronan-mediated signaling and cytoskeletal dynamics driving tumor progression.
In the HGC-27 metastatic gastric cancer model, CD44 knockout enables dissection of CD44??s role in cancer cell dissemination and stemness, processes critical for metastasis. CD44 is associated with cancer stem cell maintenance and epithelial-mesenchymal transition. Disrupting CD44 in these cells reveals its impact on cell-matrix adhesion, cytoskeletal reorganization, and signaling pathways relevant to gastric adenocarcinoma. The polyclonal knockout population avoids single-clone bias, providing a more physiologically representative loss-of-function model and facilitating identification of compensatory mechanisms.
Researchers can utilize these polyclonal knockout cells in Transwell migration and invasion assays, wound healing experiments, and hyaluronan adhesion studies to dissect CD44-dependent motility. Flow cytometry confirms CD44 surface expression loss, while western blotting detects alterations in phosphorylated AKT and ERK. RT-qPCR can quantify downstream target genes like MMP-9 and VEGF. In vivo xenograft models and drug sensitivity assays further enable investigation of CD44??s contribution to gastric cancer metastasis and chemoresistance. For additional technical information, please contact Ascent Research.
