CCM2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric cancer cell line, designed for loss-of-function studies of CCM2. The polyclonal format provides a heterogeneous mixture of cells with gene disruption, suitable for population-level assays. The targeted gene disruption was achieved via CRISPR/Cas9-mediated genome editing, enabling functional interrogation of CCM2 signaling networks in a gastric carcinoma context.
HGC-27 is a widely used cell line established from the lymph node metastasis of an undifferentiated gastric adenocarcinoma. This line retains characteristics of metastatic gastric cancer, making it a relevant model for studying tumor cell invasion, migration, and metastatic dissemination. Its undifferentiated phenotype and lymph node origin offer a platform to investigate molecular mechanisms driving aggressive gastric cancer behavior.
CCM2 encodes a scaffold protein central to the CCM complex, which includes KRIT1 and PDCD10. This complex negatively regulates MEKK3-dependent p38 MAPK activation and modulates RhoA/ROCK signaling, thereby controlling actin cytoskeleton dynamics, cell adhesion, and vascular integrity. Upstream regulators such as integrin signaling, mechanical stress, and ITGB1BP1 (ICAP1) influence CCM2 activity. Downstream effectors include MAP3K3, MAPK14, RhoA, ROCK, MLC2, and ACTA2, while interacting partners like HEG1 further fine-tune pathway output.
In the HGC-27 gastric carcinoma model, CCM2 loss is predicted to disrupt the balance of these signaling cascades, potentially enhancing cell migration and invasion??key processes in metastasis. This knockout model allows researchers to dissect CCM2-dependent regulatory mechanisms in a cancer-relevant background, extending its utility beyond cerebral cavernous malformation research to gastric cancer and vascular pathology.
Researchers can employ this knockout product in a wide array of applications, including functional studies of cell adhesion and migration using wound healing and Transwell assays, investigation of MEKK3-MAPK signaling via phospho-p38 MAPK detection, analysis of RhoA activation status, and co-immunoprecipitation to probe protein interactions with KRIT1 or PDCD10. Immunofluorescence and F-actin staining enable visualization of cytoskeletal changes. These cells are also valuable for drug target validation and preclinical assessment of therapeutics aimed at modulating CCM2-related pathways. For technical inquiries or further support, please contact Ascent Research.
