Lithium chloride increases pigmentation of melanoma cells by interfering with the inositol phosphate pathway

Kang, Hee Young; Jung, Eun Seon; Cho, Younki; Kang, Won Hyoung

doi:10.1007/s00403-002-0352-9

Cited by 2 publications

(1 citation statement)

References 11 publications

(8 reference statements)

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“…In a previous study, it was reported that lithium treatment stimulates pigmentation in embryonic zebrafish through the synthesis ⁄ deposition of melanin within the neural crest-derived melanophores (Jin and Thibaudeau, 1999). Moreover, it has been reported that exposure of B16F10 cells to LiCl results in a dose-dependent increase in the levels of differentiation-associated markers of melanoma cells such as melanin synthesis and tyrosinase activity (Kang et al, 2002). In our experiments, treatment with LiCl increased pigmentation of B16F10-mock transfected cells as shown by the gross appearance of cell pellets ( Figure 6A) and L-DOPA oxidation was also increased by LiCl treatment in B16F10-mock transfected cells ( Figure 6B).…”

Section: Ndrg2 Overexpression Inhibits Camp-induced Melanogenesismentioning

confidence: 99%

NDRG2 gene expression in B16F10 melanoma cells restrains melanogenesis via inhibition of Mitf expression

Kim

Yang

Lee

et al. 2008

Pigment Cell Melanoma Res

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Section: Ndrg2 Overexpression Inhibits Camp-induced Melanogenesismentioning

confidence: 99%

NDRG2 gene expression in B16F10 melanoma cells restrains melanogenesis via inhibition of Mitf expression

Kim

Yang

Lee

et al. 2008

Pigment Cell Melanoma Res

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Quantum Tunneling-Induced Membrane Depolarization Can Explain the Cellular Effects Mediated by Lithium: Mathematical Modeling and Hypothesis

et al. 2021

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Lithium imposes several cellular effects allegedly through multiple physiological mechanisms. Membrane depolarization is a potential unifying concept of these mechanisms. Multiple inherent imperfections of classical electrophysiology limit its ability to fully explain the depolarizing effect of lithium ions; these include incapacity to explain the high resting permeability of lithium ions, the degree of depolarization with extracellular lithium concentration, depolarization at low therapeutic concentration, or the differences between the two lithium isotopes Li-6 and Li-7 in terms of depolarization. In this study, we implemented a mathematical model that explains the quantum tunneling of lithium ions through the closed gates of voltage-gated sodium channels as a conclusive approach that decodes the depolarizing action of lithium. Additionally, we compared our model to the classical model available and reported the differences. Our results showed that lithium can achieve high quantum membrane conductance at the resting state, which leads to significant depolarization. The quantum model infers that quantum membrane conductance of lithium ions emerges from quantum tunneling of lithium through the closed gates of sodium channels. It also differentiates between the two lithium isotopes (Li-6 and Li-7) in terms of depolarization compared with the previous classical model. Moreover, our study listed many examples of the cellular effects of lithium and membrane depolarization to show similarity and consistency with model predictions. In conclusion, the study suggests that lithium mediates its multiple cellular effects through membrane depolarization, and this can be comprehensively explained by the quantum tunneling model of lithium ions.

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Lithium chloride increases pigmentation of melanoma cells by interfering with the inositol phosphate pathway

Cited by 2 publications

References 11 publications

NDRG2 gene expression in B16F10 melanoma cells restrains melanogenesis via inhibition of Mitf expression

NDRG2 gene expression in B16F10 melanoma cells restrains melanogenesis via inhibition of Mitf expression

Quantum Tunneling-Induced Membrane Depolarization Can Explain the Cellular Effects Mediated by Lithium: Mathematical Modeling and Hypothesis

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