This product consists of a CRISPR/Cas9-edited polyclonal knockout cell population of the human colorectal carcinoma cell line HCT 116, engineered for targeted disruption of the KCNJ2 gene. KCNJ2 encodes the inward rectifier potassium channel Kir2.1, a critical regulator of resting membrane potential and cellular excitability. The polyclonal knockout format provides a heterogeneous population of gene-edited cells, enabling functional studies of KCNJ2 loss without clonal selection artifacts. This model is designed for advanced biomedical research applications requiring modulation of potassium channel activity in an epithelial tumor context.
HCT 116 is an adherent, epithelial cell line derived from a human colorectal carcinoma, widely utilized as a model for colorectal cancer and epithelial tumor biology. These cells harbor an activating KRAS mutation, contributing to their transformed phenotype and relevance to oncogenic signaling studies. The cell line??s well-characterized genetic background and robust growth characteristics make it suitable for investigating the interplay between ion channel function and cancer cell behavior. In this knockout model, disruption of KCNJ2 provides a platform to explore potassium channel-dependent processes in colorectal carcinoma.
The Kir2.1 channel mediates the strong inward rectifier potassium current (IK1), stabilizing the resting membrane potential by permitting potassium influx at hyperpolarized potentials. Its activity is regulated by PIP2 and modulated by PKA and PKC phosphorylation. Kir2.1 interacts with scaffold proteins DLG1 (SAP97), CASK, and LIN7 family members, affecting trafficking and localization. Downstream, it modulates membrane hyperpolarization and indirectly regulates voltage-gated calcium channels, influencing cellular excitability.
In the context of HCT 116 colorectal carcinoma cells, knockout of KCNJ2 is hypothesized to disrupt potassium homeostasis and alter membrane potential dynamics, potentially influencing processes such as proliferation, migration, and apoptosis. Given the role of ion channels in cancer cell behavior, this model enables dissection of Kir2.1-specific contributions to tumor cell physiology. Changes in intracellular calcium signaling resulting from altered membrane potential may affect downstream pathways relevant to epithelial tumor biology. The polyclonal nature of the knockout population captures diverse editing outcomes, facilitating robust functional characterization.
This KCNJ2 knockout polyclonal cell model enables studies in cancer ion channel biology, colorectal cancer electrophysiology, and drug screening for Kir2.1 modulators. Researchers can employ patch-clamp electrophysiology, Western blotting, and RT-qPCR for target gene ablation confirmation, alongside membrane potential?Csensitive fluorescent dyes. Functional assays such as MTS proliferation, Boyden chamber migration, calcium imaging, and Annexin V apoptosis detection allow comprehensive phenotypic assessment. The model also supports investigation of Andersen-Tawil syndrome, short QT syndrome, and familial atrial fibrillation by providing a human epithelial context for Kir2.1-related pathophysiology. For additional technical information, please contact Ascent Research.
