Abstract
Voltage-gated K+ (Kv) channels are well known to be involved in cell proliferation. However, even though cell proliferation is closely related to cell differentiation, the relationship between Kv channels and cell differentiation remains poorly investigated. This study demonstrates that Kv3.3 is involved in K562 cell erythroid differentiation. Down-regulation of Kv3.3 using siRNA-Kv3.3 increased hemin-induced K562 erythroid differentiation through decreased activation of signal molecules such as p38, cAMP response element-binding protein, and c-fos. Down-regulation of Kv3.3 also enhanced cell adhesion by increasing integrin β3 and this effect was amplified when the cells were cultured with fibronectin. The Kv channels, or at least Kv3.3, appear to be associated with cell differentiation; therefore, understanding the mechanisms of Kv channel regulation of cell differentiation would provide important information regarding vital cellular processes.
Highlights
Voltage-gated K+ (Kv) channels are well-established ion channels in excitable cells, where they serve as regulators of membrane potential and neuronal activities; these channels are found in non-excitable cells, including cancer cells [1,2,3]
Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that seven different Kv channels (Kv1.2, Kv1.4, Kv2.1, Kv3.3, Kv3.4, Kv4.3, and Kv9.3) were detected in K562 cells (Fig 1A)
We first identified which Kv channel subunits exist in K562 cells and the roles of Kv channels in K562 cell differentiation
Summary
Voltage-gated K+ (Kv) channels are well-established ion channels in excitable cells, where they serve as regulators of membrane potential and neuronal activities; these channels are found in non-excitable cells, including cancer cells [1,2,3]. The modulation of certain Kv channel subunits, such as Kv1.1, Kv1.3, Kv4.1, Kv10.1, and Kv11.1, significantly affects cancer cell proliferation [8, 10,11,12,13]. K562 cells are human immortalized myelogenous leukemia cells obtained from the pleural fluid of patients with chronic myeloid leukemia in blast crisis [17]. These cells have been useful for studying hematopoietic cell proliferation and differentiation [18] and can differentiate into an erythroid lineage when treated with differentiation-inducing reagents such as hemin, sodium butyrate, and nicotinic acid [19, 20]. The induced cells produce hemoglobin, and differentiation can be validated by benzidine staining or hemoglobin quantification [18, 21,22,23]
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