The KCNK3 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the HGC-27 human gastric adenocarcinoma line, featuring targeted disruption of the KCNK3 gene. This product provides a heterogeneous pool of knockout cells, enabling robust functional studies without the confounding effects of clonal selection. The polyclonal format is particularly suited for population-level assays where the average consequence of gene inactivation is examined.
The HGC-27 cell line was originally established from a lymph node metastasis of a patient with gastric adenocarcinoma. It is extensively characterized and widely used in oncology research as a model for metastatic gastric carcinoma. HGC-27 cells display epithelial morphology and retain key oncogenic properties of the original tumor, offering a physiologically relevant system to study the molecular mechanisms underlying gastric cancer progression and therapeutic resistance.
KCNK3 encodes TASK-1, a pH-sensitive, two-pore-domain background potassium channel that is crucial for maintaining resting membrane potential. TASK-1 activity is modulated by extracellular protons, hypoxia, volatile anesthetics such as halothane, and intracellular signaling pathways involving protein kinases PKA and PKC downstream of Gq-coupled receptors. TASK-1 forms functional heterodimers with KCNK9 (TASK-3) and interacts with regulatory proteins including 14-3-3 isoforms, ??-COP, and the actin cytoskeleton. By setting the resting potential, TASK-1 indirectly controls the gating of voltage-gated calcium channels, thereby regulating intracellular calcium levels and the activity of the calcineurin/NFAT and CREB transcriptional pathways. These downstream effectors influence expression of genes controlling cell cycle progression and apoptosis.
In the context of gastric cancer, KCNK3 expression has been linked to cellular behaviors such as proliferation, migration, and survival. Disruption of TASK-1 in HGC-27 cells is expected to cause membrane depolarization, leading to increased calcium influx and aberrant activation of calcium-dependent signaling cascades. This polyclonal loss-of-function model provides a powerful tool to dissect the contribution of TASK-1 to gastric adenocarcinoma pathophysiology, circumventing artifacts that may arise from single-cell cloning.
This knockout cell product is designed for diverse research applications, including probing the role of background potassium currents in cancer cell biology, screening pharmacological modulators of TASK-1 for pulmonary arterial hypertension, and performing electrophysiological analyses via patch clamp. Researchers can validate knockout efficiency with western blotting, RT-qPCR, and immunofluorescence, and subsequently assess functional impacts using MTT proliferation assays, Transwell migration/invasion assays, Annexin V apoptosis staining, calcium imaging, and drug sensitivity profiling. The KCNK3 Knockout HGC-27 Polyclonal Cells offer a versatile and reliable platform for both mechanistic studies and drug discovery. For further inquiries, please contact Ascent Research.
