The KCNJ2 Knockout TE1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of TE1 human esophageal squamous cell carcinoma cells with targeted disruption of the KCNJ2 gene. This loss-of-function model is generated via CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of edited alleles that eliminates functional Kir2.1 protein expression. The polyclonal format provides a versatile tool for studying the collective impact of KCNJ2 deletion without clonal isolation, suitable for pooled phenotypic screening and population-level analyses of inward rectifier potassium channel function.
TE1 is a human esophageal squamous cell carcinoma line established from a well-differentiated tumor, displaying adherent epithelial morphology and malignant properties such as uncontrolled proliferation and migration. It serves as a clinically relevant model for esophageal cancer research, endogenously expressing KCNJ2 and enabling investigation of ion channel contributions to oncogenic processes.
KCNJ2 encodes Kir2.1, an inward rectifier potassium channel that stabilizes resting membrane potential by mediating potassium influx. Its activity is regulated by PIP2, PKA, PKC, and ??-adrenergic signaling, with transcription controlled by SP1. Knockout eliminates Kir2.1 current, causing membrane depolarization, altered calcium dynamics, and attenuated ERK1/2 and AKT phosphorylation, leading to reduced cyclin D1 and MMP-9 expression and impaired cell cycle progression and migration. Kir2.1 interacts with scaffolding proteins including DLG1/SAP97, caveolin-3, and PSD-95, which organize channel complexes at the membrane.
In esophageal squamous cell carcinoma, KCNJ2 knockout in TE1 cells reveals the functional role of Kir2.1 in sustaining proliferative and migratory signaling through ERK1/2?CAKT pathways. This model allows dissection of how ion channel-mediated membrane potential regulation influences calcium signaling, gene expression, and drug sensitivity, highlighting potential vulnerabilities in cancer cells.
Applications include western blotting and RT-qPCR for verifying KCNJ2 disruption and downstream targets, patch-clamp electrophysiology to confirm loss of inward rectifier currents, and proliferation assays (MTT/CCK-8). Migration can be assessed by wound healing and transwell assays, complemented by calcium imaging with Fluo-4 and flow cytometry for cell cycle analysis. The polyclonal format supports RNA-seq transcriptome profiling and drug sensitivity screens (e.g., cisplatin) for target validation and ion channel modulator discovery. For additional information, please contact Ascent Research.
