The anti-proliferative effect of lithium chloride on melanoma cells and its reversion by myo-inositol

Nordenberg, Jardena; Panet, C.; Wasserman, Lina; Malik, Zvi; Fuchs, Anna‐Riitta; Stenzel, K. H.; Novogrodsky, Abraham

doi:10.1038/bjc.1987.9

Cited by 21 publications

(6 citation statements)

References 30 publications

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“…This hypothesis is consistent with theoretical models predicting a higher probability of the Crabtree effect in the case of decreased permeability of the mitochondrial voltage-dependent anion channel and a high amount of hexokinase II attached to the outer mitochondrial membrane (30,31). Lithium chloride, which has an anti-proliferative effect on melanoma cells (32), induces detachment of hexokinase from mitochondria (33), and vice versa, the interaction of hexokinase II with voltage-dependent anion channel inhibits the release of cytochrome c from mitochondria induced by pro-apoptotic protein Bax (34). In this sense some synthetic polycation peptides are also able to inhibit the mitochondrial permeability transition (35).…”

supporting

confidence: 76%

Mitochondria Permeabilization by a Novel Polycation Peptide BTM-P1

Lemeshko

Arias

Ordúz

2005

Journal of Biological Chemistry

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Bacillus thuringiensis subsp. medellin is known to produce the Cry11Bb protein of 94 kDa, which is toxic for mosquito larvae due to permeabilization of the plasma membrane of midgut epithelial cells. Earlier we found that a 2.8-kDa novel peptide BTM-P1, which was artificially synthesized taking into account the primary structure of Cry11Bb endotoxin, is active against several species of bacteria. In this work we show that BTM-P1 induces cyclosporin A-insensitive swelling of rat liver mitochondria in various salt solutions but not in the sucrose medium. Inorganic phosphate and Ca 2؉ significantly increased this effect of the peptide. The uncoupling action of BTM-P1 on oxidative phosphorylation was stronger in the potassiumcontaining media and correlated with a decrease of the inner membrane potential of mitochondria. In isotonic KNO 3 , KCl, or NH 4 NO 3 media, a complete drop of the inner membrane potential was observed at 1-2 g/ml of the peptide. The peptide-induced swelling was increased by energization of mitochondria in the potassium-containing media, but it was inhibited in the NaNO 3 , NH 4 NO 3 , and Tris-NO 3 media. All mitochondrial effects of the peptide were completely prevented by adding a single N-terminal tryptophan residue to the peptide sequence. We suggest a mechanism of membrane permeabilization that includes a transmembrane-and surface potential-dependent insertion of the polycation peptide into the lipid bilayer and its oligomerization leading to formation of ion channels and also to the mitochondrial permeability transition pore opening in a cyclosporin A-insensitive manner.

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confidence: 76%

Mitochondria Permeabilization by a Novel Polycation Peptide BTM-P1

Lemeshko

Arias

Ordúz

2005

Journal of Biological Chemistry

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“…As shown in Fig. 1E, the cell numbers in the presence of 3 or 10 mM LiCl decreased to 61.48± 13.42% and 31.29±8.25% (n=5, P<0.01) of the control (100%), respectively, which is consistent with the observation of Nordenberg et al [4]. It is highly likely that the differentiation of melanoma cells in the presence of LiCl was the cause of the induction of tyrosinase to synthesize melanin.…”

Section: Licl Stimulates Pigmentation In Melanoma Cellssupporting

confidence: 80%

“…Interestingly, in embryonic zebra fish, LiCl can cause a dramatic increase in the appearance of pigmentation [3]. In melanoma cells, it has been demonstrated that LiCl inhibits cell growth and delays the appearance of tumors in mice [4]. As in the case of remission of vitiligo during lithium salt medication, it seems that LiCl stimulates pigmentation of skin [5].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2002

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“…Wennersten Jimbow & Vesugi, 1982. NADPH cytochrome c reductase was recently found to be increased in B16 melanoma cells following treatment with LiCI (Nordenberg et al, 1987) and derivatives of dimethylthiourea (unpublished data). These agents also inhibit melanoma cell growth and induce several differentiated features in these cells.…”

Section: Resultsmentioning

confidence: 99%

Biochemical and ultrastructural alterations accompany the anti-proliferative effect of butyrate on melanoma cells

Nordenberg¹,

Wasserman²,

Peled³

et al. 1987

Br J Cancer

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Summary The effect of sodium butyrate on mouse and human melanoma cell lines was evaluated. Sodium butyrate (0.1-2mM) is shown to reduce the clonogenic potential of several melanoma cell lines. The antiproliferative effect of sodium butyrate is accompanied by a marked increase in the activity of the plasmamembrane bound enzyme y-glutamyl transpeptidase. Sodium butyrate treated cells acquire a well developed rough endoplasmic reticulum and accumulate fat droplets. The development of the endoplasmic reticulum is associated with a marked increase in the activity of the enzyme marker NADPH cytochrome c reductase. It is suggested that the phenotypic alterations induced by sodium butyrate may serve as markers for the action of this agent on melanoma cells and other tumours.Butyric acid, a natural four carbon fatty acid, is known as an inducer of differentiation in Friend erythroleukaemic cells (Leder & Leder, 1975;Reeves & Cserjesi, 1979). In vivo application of sodium butyrate to a child with acute myelogenous leukaemia resulted in a partial remission (Novogrodsky et al., 1983).Butyric acid (or its sodium salt) also induce phenotypic alterations in a variety of solid tumour cell lines such as Hela cells (Fishman et al., 1974;Gosh & Cox, 1976), neuroblastoma (Prasad, 1979;Rama & Prasad, 1984), breast cancer cells (Abe & Kufe, 1984;Stevens et al., 1984, colorectal carcinoma (Dexter et al., 1981;Kim et al., 1980; Hertz & Halwer, 1982) and retinoblastoma (Kyritsis et al., 1984). The anti-tumour effects of sodium butyrate that include growth inhibition and decrease in tumorigenicity (for review see Prasad, 1980; Wright, 1973;Leavitt et al., 1978;Reese et al., 1985; Nordenberg et al., 1986a, b) are accompanied by changes in enzyme activities (Simmons et al., 1975;Prasad, 1980;Dexter et al., 1981;Prager & Kanar, 1984), receptor content (Fishman & Atikkan, 1979;Jahangeer et al., 1982) and histone structure (Sealy & Chulkley, 1978;Rubenstein et al., 1979).We have recently shown that sodium butyrate markedly inhibits B 16 mouse melanoma cell growth and alters the morphologic appearance of these cells. Growth inhibition was accompanied by a marked inhibition of tyrosinase activity (Nordenberg et al., 1986a).In the present study we further evaluate the effects of sodium butyrate on mouse melanoma cells and expand our studies to human malignant melanoma cells. Sodium butyrate is shown to inhibit clonogenicity of the different melanoma cells in soft agar. This anti-proliferative effect of sodium butyrate is associated with a marked increase in the activities of the plasma membrane bound enzyme y-glutamyl transpeptidase and NADPH cytochrome c reductase, a marker of the well developed endoplasmic reticulum.These phenotypic alterations may serve as markers for butyrate activity on melanoma cells in basic and clinical studies.

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The anti-proliferative effect of lithium chloride on melanoma cells and its reversion by myo-inositol

Cited by 21 publications

References 30 publications

Mitochondria Permeabilization by a Novel Polycation Peptide BTM-P1

Mitochondria Permeabilization by a Novel Polycation Peptide BTM-P1

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

Biochemical and ultrastructural alterations accompany the anti-proliferative effect of butyrate on melanoma cells

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