The KCNJ2 Knockout HGC-27 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population derived from the HGC-27 human gastric carcinoma cell line, carrying a targeted disruption of the KCNJ2 gene. This loss-of-function model facilitates the study of Kir2.1 inward rectifier potassium channel function in a gastric cancer background. The polyclonal format, generated by CRISPR/Cas9-mediated gene disruption, provides a heterogeneous editing spectrum that avoids clonal artifacts commonly associated with single-cell-derived knockouts.
HGC-27 is an epithelial tumor line established from a lymph node metastasis of an undifferentiated gastric carcinoma. It retains aggressive properties including invasive and migratory capacity, serving as a widely used in vitro system for gastric cancer progression research. The cellular context is particularly relevant for interrogating ion channel contributions to metastasis and tumorigenesis.
KCNJ2 encodes Kir2.1, a strong inward rectifier potassium channel that stabilizes resting membrane potential and maintains potassium homeostasis. Kir2.1 is activated by PIP2 and regulated by PKA and tyrosine kinases downstream of beta-adrenergic signals. The channel interacts with scaffolding proteins MAGI-1, DLG1 (SAP97), and CASK, forming complexes that link membrane potential to intracellular pathways. Knockout of KCNJ2 depolarizes the cell membrane, alters calcium influx, and disrupts downstream targets including AKT and MAPK1. This results in modulation of cell cycle regulators and impacts Wnt and MAPK signaling cascades, collectively affecting proliferation and migration.
In gastric cancer, KCNJ2 expression changes have been associated with tumor progression. The HGC-27 knockout model enables dissection of Kir2.1-dependent effects on cell cycle, apoptosis, and metastatic potential. Additionally, KCNJ2 mutations are linked to Andersen-Tawil syndrome, short QT syndrome type 3, and atrial fibrillation, highlighting its broad physiological importance beyond oncology. This polyclonal knockout population offers a robust tool to study ion channel-driven mechanisms in gastric carcinoma.
Typical assays for this model include patch clamp electrophysiology to measure potassium currents, Western blotting for Kir2.1 protein, proliferation assays (MTT/BrdU), Transwell migration/invasion studies, calcium imaging, and RNA-seq transcriptomics. Research applications encompass elucidating potassium channel roles in gastric cancer, validating drug targets, and investigating crosstalk with AKT and MAPK pathways. This product supports advanced cancer signaling and drug discovery studies. For additional technical details or custom gene editing services, please contact Ascent Research.
