Description

The STON2 Knockout 6-10B Cell Line is a CRISPR/Cas9-edited knockout cell line originating from the human 6-10B gastric adenocarcinoma cell line, with targeted disruption of the STON2 gene. This gene-edited product eliminates functional stonin-2 protein, creating a loss-of-function model for investigating endocytic adaptor proteins in cancer cell biology. The knockout is achieved through CRISPR/Cas9-mediated gene disruption, providing a stable and specific experimental system to study STON2-dependent processes without the variability of transient approaches.

The 6-10B host cell line was established from a metastatic lymph node of a gastric adenocarcinoma patient and serves as a widely recognized model for gastric cancer metastasis research. It retains aggressive properties including invasive and migratory capacity, making it particularly suitable for dissecting the molecular underpinnings of cancer dissemination. This cell line has been extensively employed in studies of epithelial-mesenchymal transition, chemoresistance, and receptor tyrosine kinase signaling, offering a clinically relevant background for functional knockout studies.

STON2 encodes an endocytic adaptor protein that bridges cargo molecules to the AP-2 complex (AP2M1, AP2B1) for clathrin-mediated endocytosis. It directly interacts with clathrin, synaptotagmin (SYT1), epsin (EPS15), and intersectin (ITSN1), orchestrating the internalization of receptors such as EGFR. STON2 disruption impairs receptor endocytosis, leading to enhanced surface receptor retention and sustained activation of downstream pathways including MAPK/ERK and PI3K/AKT. The mechanistic network also involves RAB5A and dynamin-2 (DNM2), which regulate early endosome formation. Consequently, STON2 ablation perturbs receptor trafficking homeostasis, with potential consequences for cell proliferation, survival, and invasive signaling.

In gastric adenocarcinoma, dysregulation of endocytic trafficking is increasingly recognized as a driver of oncogenic signaling and therapeutic resistance. The STON2 Knockout 6-10B Cell Line allows systematic evaluation of how loss of an endocytic adaptor reshapes the cell surface receptor proteome and intracellular kinase networks in a metastatic context. This model is particularly useful for examining STON2-dependent regulation of EGFR stability and signaling output, and for probing how endocytic deficiency may promote compensatory mechanisms that enhance metastatic behavior. Such studies can pinpoint molecular vulnerabilities for therapeutic intervention.

This knockout cell line supports diverse assays including quantitative flow cytometry for surface receptor measurement, immunofluorescence microscopy for receptor localization, and fluorescent ligand uptake assays to monitor endocytosis kinetics. It is also suitable for drug sensitivity profiling with targeted agents, proliferation, migration, and invasion assays, as well as global transcriptomic analysis via RNA-seq. The model serves as a vital tool for advancing research in cancer cell biology, receptor trafficking, and the development of endocytosis-directed therapies. For additional information, please contact Ascent Research.