This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma epithelial cell line HGC-27, engineered to disrupt the CD320 gene. CD320 encodes the receptor for transcobalamin-bound cobalamin (vitamin B12), and its targeted disruption enables investigation of B12-dependent processes in a gastric cancer model. The polyclonal knockout pool provides a heterogeneous loss-of-function model that avoids assumptions of clonal homogeneity and is suitable for functional studies requiring population-level analyses.
The HGC-27 host cell line is an undifferentiated gastric adenocarcinoma cell line originally isolated from a lymph node metastasis of a poorly differentiated gastric carcinoma. This cell line is a widely utilized model for metastatic gastric cancer, retaining aggressive growth characteristics and serving as a platform to study oncogenic signaling, metabolic adaptation, and therapeutic vulnerabilities. Its gastric origin is particularly relevant for examining nutrient uptake pathways and their roles in tumorigenesis.
CD320 functions as a cell surface receptor for the TCN2-bound cobalamin complex, mediating its internalization via endocytosis. Upon lysosomal release, cobalamin acts as a cofactor for methionine synthase (MTR) and methylmalonyl-CoA mutase (MUT), linking vitamin B12 availability to one-carbon metabolism, homocysteine remethylation, and nucleotide synthesis. Transcription of CD320 is regulated by MYC and HIF1A, and its activity influences cellular methylation potential and DNA synthesis. Interaction with CUBN and the TCN2-B12 complex is essential for efficient cobalamin uptake, placing CD320 at the nexus of nutrient sensing and metabolic control.
In the context of HGC-27 gastric cancer cells, knockout of CD320 provides a defined model to dissect the reliance of tumor cells on exogenous cobalamin for sustaining proliferation and epigenetic integrity. Given the aggressive nature of this metastatic line, the CD320-disrupted population can be used to test whether impaired B12 uptake sensitizes cells to metabolic stress, chemotherapy, or targeted agents. This model is particularly valuable for exploring synthetic lethal interactions and the role of one-carbon metabolism in gastric adenocarcinoma progression.
Researchers can employ this knockout model for a range of applications, including B12 uptake assays to confirm receptor dependency, proliferation studies under cobalamin deprivation to assess metabolic vulnerabilities, and global DNA methylation profiling to investigate epigenomic consequences. Additional assays such as homocysteine and methylmalonic acid quantification facilitate direct readouts of pathway disruption. Transcriptomic analysis via RNA-seq enables deeper exploration of compensatory mechanisms, while flow cytometry confirms surface CD320 loss. These applications support drug target validation and functional genomics studies in gastric cancer. For further details on this knockout product, please contact Ascent Research.
