Melanoma Cell Signalling: Looking Beyond RAS-RAF-MEK

Muthusamy, Visalini; Piva, Terrence J.

doi:10.5772/26725

Cited by 4 publications

(11 citation statements)

References 113 publications

(165 reference statements)

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“…Following treatment of cells with the indicated compound at 10 µM or ethanol (0.1%, v/v) for 18 h, cell lysates were prepared and an aliquot of each sample (10 μg per lane) was resolved by 8% SDS-PAGE, transferred to a PDVF membrane, and probed with anti-β-tubulin (1:2000), anti-PHIP (1:2000), or anti-β-actin (1:5000) (loading control), followed by HRP-conjugated anti-rabbit secondary antibody and chemiluminescence detection. The results are representative of three independent experiments.…”

Section: Chartmentioning

confidence: 99%

“…C. Western blot analysis of lysates (50 µg protein per lane) that had been prepared from cells treated for 18 h with 10 µM of the indicated analogue. The blot was probed with anti-β-tubulin (1:2000) or anti-β-actin (1:5000) followed by HRP-conjugated secondary antibody and detected by chemiluminescence. The results are representative of three independent experiments.…”

Section: Chartmentioning

confidence: 99%

“…In view of the rising incidence of melanoma over the past decade, research has focused on approaches using drugs that would prevent metastasis of the primary lesion (1). In recent years, activating mutations of B-raf and N-ras were implicated in mechanisms that drive proliferation and metastasis of 50% of human melanomas (2).…”

Section: Introductionmentioning

confidence: 99%

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Anti-tumor properties of cis-resveratrol methylated analogs in metastatic mouse melanoma cells

et al. 2015

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Resveratrol (E-3,5,4’-trihydroxystilbene) is a polyphenol found in red wine that has been shown to have multiple anti-cancer properties. Although cis (Z) and trans (E) isomers of resveratrol occur in nature, the cis form is not biologically active. However, methylation at key positions of the cis form results in more potent anti-cancer properties. This study determined that synthetic cis-polymethoxystilbenes (methylated analogues of cis-resveratrol) inhibited cancer-related phenotypes of metastatic B16 F10 and non-metastatic B16 F1 mouse melanoma cells. In contrast with cis or trans-resveratrol and trans-polymethoxystilbene which were ineffective at 10 μM, cis-polymethoxystilbenes inhibited motility and proliferation of melanoma cells with low micromolar specificity (IC50 <10 μM). Inhibitory effects by cis-polymethoxystilbenes were significantly stronger with B16 F10 cells and were accompanied by decreased expression of β-tubulin and pleckstrin homology domain-interacting protein, a marker of metastatic B16 cells. Thus, cis-polymethoxystilbenes have potential as chemotherapeutic agents for metastatic melanoma.

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Section: Chartmentioning

confidence: 99%

Section: Chartmentioning

confidence: 99%

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Anti-tumor properties of cis-resveratrol methylated analogs in metastatic mouse melanoma cells

et al. 2015

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“…The carcinogenic stimulus, ultraviolet (UV) radiation, can transform melanocytes into melanomas, which are an aggressive malignant skin cancer [1,2]. Both UVA and UVB radiation can penetrate into the epidermis and initiate molecular interactions leading to UV-induced responses.…”

Section: Introductionmentioning

confidence: 99%

“…Some of these molecular interactions can give rise to genetic alteration, activation/suppression of cell signaling pathways, resulting in either the upregulation or downregulation of cytokine release. The molecular interactions of the B-Raf/extracellular-signal regulated kinase (ERK) pathway in melanoma cells have been widely investigated [1–3]. Unlike ERK, the other mitogen-activated protein kinase (MAPK); p38 MAPK and c-jun terminal kinase (JNK), and nuclear factor-κB (NFκB) pathways have not been frequently linked to melanoma incidences [1].…”

Section: Introductionmentioning

confidence: 99%

UVB-Stimulated TNFα Release from Human Melanocyte and Melanoma Cells Is Mediated by p38 MAPK

Muthusamy

Piva

2013

IJMS

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Ultraviolet (UV) radiation activates cell signaling pathways in melanocytes. As a result of altered signaling pathways and UV-induced cellular damage, melanocytes can undergo oncogenesis and develop into melanomas. In this study, we investigated the effect of UV-radiation on p38 MAPK (mitogen-activated protein kinase), JNK and NFκB pathways to determine which plays a major role in stimulating TNFα secretion in human HEM (melanocytes) and MM96L (melanoma) cells. MM96L cells exhibited 3.5-fold higher p38 activity than HEM cells at 5 min following UVA + B radiation and 1.6-fold higher JNK activity at 15–30 min following UVB+A radiation, while NFκB was minimally activated in both cells. Irradiated HEM cells had the greatest fold of TNFα secretion (UVB: 109-fold, UVA + B: 103-fold & UVB+A: 130-fold) when co-exposed to IL1α. The p38 inhibitor, SB202190, inhibited TNFα release by 93% from UVB-irradiated HEM cells. In the UVB-irradiated MM96L cells, both SB202190 and sulfasalazine (NFκB inhibitor) inhibited TNFα release by 52%. Although, anisomycin was a p38 MAPK activator, it inhibited TNFα release in UV-irradiated cells. This suggests that UV-mediated TNFα release may occur via different p38 pathway intermediates compared to those stimulated by anisomycin. As such, further studies into the functional role p38 MAPK plays in regulating TNFα release in UV-irradiated melanocyte-derived cells are warranted.

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