The EFHD1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which EFHD1 has been disrupted to generate a loss-of-function model. This product offers a defined genetic background for investigating EFHD1??s roles in apoptosis and mitochondrial regulation. The polyclonal nature captures diverse editing events, providing a robust system for functional studies without clonal selection bias. Researchers can dissect EFHD1-mediated signaling networks and their contributions to oncogenic phenotypes.
The host HGC-27 cell line is a human gastric carcinoma epithelial line derived from lymph node metastasis of a gastric adenocarcinoma patient. It serves as a clinically relevant model for gastric cancer biology, including metastatic progression and therapeutic resistance. HGC-27 cells exhibit dysregulated proliferation and apoptosis pathways, making them suitable for evaluating tumor suppressor functions. Their genetic accessibility enables targeted exploration of genes implicated in gastrointestinal cancers.
EFHD1 encodes a calcium-binding protein that localizes to mitochondria and regulates membrane permeability and apoptotic cell death. It interacts with VDAC and AIFM1, modulating cytochrome c release and caspase activation. EFHD1 functions downstream of calcium ion fluxes and potential inputs from p53 and stress signals. Acting as a scaffold, it integrates calcium signaling with the mitochondrial apoptosis pathway, influencing BCL2 family members. Disruption of EFHD1 perturbs calcium-dependent mitochondrial checkpoint control, altering sensitivity to intrinsic apoptotic stimuli.
In HGC-27 cells, loss of EFHD1 may mimic tumor conditions with downregulated EFHD1 expression. As a proposed tumor suppressor, its knockout can reveal mechanisms of apoptosis evasion and calcium dysregulation in gastric carcinogenesis. This model dissects EFHD1??s role in mitochondrial integrity and cell death, offering insights into chemoresistance and metastatic behavior. The interplay among EFHD1, PI3K/Akt signaling, and mitochondrial apoptosis can be systematically studied to identify therapeutic vulnerabilities.
This knockout population is suitable for western blotting of apoptosis markers, flow cytometry (Annexin V/PI), mitochondrial membrane potential assays, calcium imaging, and cell viability assays. Researchers investigating calcium-dependent apoptosis, mitochondrial dysfunction in cancer, or tumor suppression will find this model valuable for mechanistic and translational studies. For further information, contact Ascent Research.
