The KCNK3 Knockout MCF-7 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human MCF-7 breast adenocarcinoma cell line, in which the KCNK3 gene encoding the TASK-1 potassium channel has been disrupted. This polyclonal knockout model is designed for loss-of-function studies of the pH- and hypoxia-sensitive two-pore domain potassium channel in a breast cancer context. The use of a polyclonal population avoids clonal biases and provides a heterogeneous knockout pool suitable for functional and pharmacological characterization of TASK-1-dependent phenotypes.
MCF-7 is a well-established human breast adenocarcinoma cell line originally isolated from a pleural effusion of a metastatic mammary carcinoma. These cells are characterized by estrogen receptor positivity, progesterone receptor positivity, and lack of HER2 amplification, classifying them as luminal A subtype. MCF-7 cells retain epithelial morphology and are widely used as a model system for hormone-responsive breast cancer. Their stable genomic background and ease of culture make them a preferred host for genetic perturbations aimed at dissecting signaling pathways relevant to breast tumor biology.
TASK-1 (K2P3.1) encoded by KCNK3 functions as a leak potassium channel that critically regulates resting membrane potential and cellular excitability. Its activity is modulated by a network of signaling inputs: it is inhibited downstream of Gq-coupled receptors through phospholipase C and protein kinase C, and its function is sensitive to extracellular pH and hypoxia. The channel interacts with 14-3-3 proteins and the adaptor p11 (S100A10), which influence trafficking and membrane retention. Loss of KCNK3 in MCF-7 cells eliminates TASK-1-mediated background potassium currents, leading to membrane depolarization and altered downstream signaling cascades that impact cell proliferation, apoptosis, and cell cycle progression.
In the context of MCF-7 breast cancer cells, TASK-1 has been implicated in regulating apoptotic sensitivity, proliferation rates, and cellular responses to the hypoxic tumor microenvironment. Disruption of KCNK3 expression in this luminal A background provides a unique model to investigate how electrical signaling and pH sensing intersect with hormone receptor signaling. The polyclonal knockout population allows researchers to study overall gene function without the confounding effects of clonal adaptation, enabling robust analysis of ion channel contributions to cancer cell physiology and therapeutic resistance mechanisms.
This knockout product is ideally suited for a range of experimental applications including ion channel pharmacology screening using patch-clamp electrophysiology, membrane potential measurements with fluorescent dyes, and proliferation (MTT) or apoptosis (Annexin V) assays. It can be used in transcriptomic studies via RNA-seq or qPCR to identify TASK-1-dependent gene networks, as well as in hypoxia response studies and drug efficacy testing. For further information or to request a quote, please contact Ascent Research.
