The CAV1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CAV1 gene in the human gastric carcinoma cell line HGC-27. This loss-of-function model enables systematic investigation of caveolin-1-dependent processes without assuming a specific editing outcome. The polyclonal format provides a robust representation of gene disruption across the population, making it a versatile tool for studying CAV1’s role in gastric cancer biology and associated signaling networks.
The host cell line HGC-27 is a gastric adenocarcinoma-derived epithelial cell line established from a human gastric carcinoma. It retains epithelial morphology and exhibits tumorigenic properties, making it widely used for studying gastric cancer progression, including mechanisms of cell proliferation, adhesion, migration, and invasion. This cell line serves as an appropriate system for exploring signaling pathways implicated in gastric carcinogenesis and therapeutic resistance.
Caveolin-1, encoded by CAV1, is the main structural component of caveolae, functioning as a scaffold that organizes membrane microdomains and recruits signaling molecules. It interacts with cavin family proteins (PTRF/cavin-1, cavin-2) and partners such as EGFR, Src, integrins, Ras, and G-proteins. Activated by EGF, PDGF, TGF-beta, TNF-alpha, and integrin engagement, CAV1 regulates downstream effectors including MAPK1/3, Akt1, eNOS, STAT3, RhoA, and Rac1. This positions CAV1 at the intersection of caveolae-mediated endocytosis, integrin signaling, TGF-beta, MAPK/ERK, PI3K-Akt, and Src pathways, coupling membrane organization to cell growth, survival, and motility.
In HGC-27 gastric cancer cells, loss of CAV1 eliminates caveolae structures, disrupting membrane organization and impairing endocytic trafficking and signal compartmentalization. This dysregulation alters growth factor receptor internalization, such as EGFR, and integrin-mediated adhesion, leading to aberrant activation of MAPK1/3 and Akt1. Consequently, CAV1 knockout can modify cellular proliferation, migration, and invasive capacity, offering a means to dissect the dual tumor-suppressive and oncogenic roles attributed to caveolin-1 in gastric carcinoma. The model thus provides insights into how caveolar disruption influences cancer cell behavior and response to microenvironmental cues.
Researchers can utilize this model for gastric cancer mechanistic investigations, cell signaling pathway analysis, migration and invasion assays, drug resistance profiling, and tumor microenvironment studies. Representative assays include western blotting for CAV1 and downstream targets (p-ERK, p-Akt), RT-qPCR for transcript quantification, immunofluorescence to visualize caveolae and CAV1, Boyden chamber migration/invasion assays, and co-immunoprecipitation of CAV1 with EGFR or Src. Flow cytometry enables integrin expression analysis. For further technical details, contact Ascent Research.
