The CAV2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-mediated knockout model targeting the human CAV2 gene in a gastric carcinoma background. This polyclonal population comprises a mixture of HGC-27 cells carrying diverse loss-of-function edits, avoiding clonal bias and preserving biological variability. Endogenous CAV2 disruption is achieved via Cas9 and guide RNA, resulting in a stable knockout suitable for pooled screening and signaling studies. Caveolin-2 protein expression is markedly reduced across the bulk culture, enabling functional analysis without single-clone artifacts, while maintaining expression of other caveolar components under endogenous regulatory control.
HGC-27 is a human gastric adenocarcinoma cell line derived from a lymph node metastasis of an undifferentiated signet ring cell carcinoma. These adherent epithelial cells harbor a mutant TP53 gene, a common feature of advanced gastric cancers. Widely used in gastrointestinal oncology, HGC-27 serves as a model for studying invasion, metastasis, and drug resistance. Its metastatic origin makes it particularly suitable for investigating molecular mechanisms of lymphatic dissemination. The CAV2 knockout in this background provides a clinically relevant system to examine caveolar dysfunction in aggressive gastric cancer.
Caveolin-2 (CAV2) encodes a scaffolding protein that forms hetero-oligomers with caveolin-1 (CAV1) within caveolae membrane invaginations. The CAV1?CCAV2 complex regulates endocytosis, lipid trafficking, and signal transduction. Transcriptionally, CAV2 is activated by TGF-??, EGF, STAT3, and HIF1A. At the protein level, it scaffolds ITGB1, EGFR, SRC, and NOS3. CAV2 deficiency alters downstream effectors including ERK1/2 (MAPK1/3), AKT1, CTNNB1, and RHOA. In the MAPK/ERK and PI3K/AKT pathways, CAV2 modulates integrin- and growth factor?Cdriven phosphorylation. Additionally, CAV2 interacts with TGFBR1 and SMAD3, integrating adhesion and migratory signals. Thus, CAV2 knockout disrupts these scaffolding interactions, deregulating signal compartmentalization and transcriptional outputs.
In HGC-27 gastric cancer cells, CAV2 loss impairs caveolae formation and integrin-mediated adhesion, leading to altered cell migration and invasion potential. Disrupted CAV2?CCAV1 scaffolding attenuates AKT and ERK signaling, potentially sensitizing cells to therapeutics. The TP53-mutant background cooperates with CAV2 deficiency to affect cell cycle and apoptosis, modeling aggressive disease. This system enables dissection of caveolin-2??s context-dependent pro- or anti-tumorigenic roles in gastric carcinogenesis.
Applications include immunofluorescence for caveolae localization, Western blotting for phospho-ERK/AKT, Transwell migration/invasion assays, and co-immunoprecipitation of CAV1. Drug sensitivity testing and RNA-seq transcriptomic profiling further link CAV2 status to gastric cancer behaviors. This polyclonal knockout model is ideal for tumor microenvironment studies and high-content screening. For further details or to request a quote, please contact Ascent Research.
