Specificity of photosensitizer accumulation in undifferentiated versus differentiated colon carcinoma cells

Siboni, Galit; Amit-Patito, I; Weizman, Efrat; Waintraub-Porat, M; Weitman, Hana; Ehrenberg, Benjamin; Malik, Zvi

doi:10.1016/s0304-3835(03)00207-6

Cited by 25 publications

(13 citation statements)

References 17 publications

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“…It is known that most types of malignant cells accumulate more ALA-induced PpIX than the normal cells from which they arose and that changes in differentiation state are celltype specific. Furthermore, the relationship between tumour cell differentiation and photo-sensitizer accumulation is poorly defined (35). Some differentiation agents, such as butyrate, did not enhance PpIX accumulation whereas others, such as hexamethylene bisacetamide (HMBA) and methotrexate, did (22,36).…”

Section: Discussionmentioning

confidence: 99%

Chrysin-induced apoptosis is mediated through p38 and Bax activation in B16-F1 and A375 melanoma cells

Canini

2011

Int J Oncol

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Abstract. Chrysin (5,7-dihydroxyflavone) is a natural and biologically active compound extracted from honey, plants and propolis. It possesses anti-inflammatory activity, antioxidant properties and promotes cell death by perturbing cell cycle progression. In this study, our attention focused on the possible role that chrysin may have as a potential anti-cancer agent, and we tested its biological activity in murine and human melanoma cell lines (B16-F1 and A375). This study demonstrated that chrysin reduced melanoma cell proliferation and induced cell differentiation in both human and murine melanoma cells through synthesis increase and intracellular accumulation of protoporphirin IX (PpIX). Furthermore, following treatments with chrysin an increase in the expression of porphobilinogen deaminase (PBG-D) was noted. This study demontrated also that chrysin induces cell death in human and murine melanoma cells through caspase-dependent mechanisms, involving down-regulation of ERK 1/2, and activation of p38 MAP kinases. Induction of cell death may be a promising therapeutic approach in cancer therapy. Our results suggest that chrysin may be considered a potential candidate for both cancer prevention and treatment.

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Section: Discussionmentioning

confidence: 99%

Chrysin-induced apoptosis is mediated through p38 and Bax activation in B16-F1 and A375 melanoma cells

Canini

2011

Int J Oncol

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“…PpIX is considered a differentiation marker for some cancer cell lines including B16 cells, since the induction of differentiation enhanced accumulation of the compound (42)(43)(44), although the relationship between tumor cell differentiation and photosensitizer accumulation is poorly defined (45). Furthermore, it is known that PpIX induces melanogenesis through the cAMP-mediated pathway; it activates the soluble guanylate cyclase and elevates intra-cellular cGMP (cyclic guanine monophosphate) content which was demonstrated to increase cAMP content by inhibition of cAMP phosphodiesterase (20,21).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Mek 1/2 kinase activity and stimulation of melanogenesis by 5,7-dimethoxycoumarin treatment of melanoma cells

Alesiani

Cicconi²,

Mattei³

et al. 2009

Int J Oncol

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Abstract. In this study, the processes of differentiation and melanogenesis induced by 5,7-dimethoxycoumarin in murine (B16) and human (A375) melanoma cells were investigated.Taking into account the previously demonstrated antiproliferative and differentiation activities of this compound, we examined Ras/Raf/Mek/Erk mitogen-activated protein kinase activity following treatment; inhibition of Mek 1/2 kinase activity and subsequent reduction in Erk 1/2 activation were detected in both cell types. We observed melanogenesis induction associated to an increase in cAMP-response elementbinding protein (CREB) and microphthalmia-associated transcription factor (Mitf) expression, both involved in its regulation. Mitf is fundamental for development, survival and differentiation of melanocyte and melanoma, since it regulates transcription of genes encoding for proteins involved in cell cycle progression or in melanogenesis, such as the enzyme tyrosinase. A significant increase of tyrosinase activity was revealed following treatment in B16 but not in A375 cells, although a strong synthesis of melanin was induced by 5,7-dimethoxycoumarin in both cell lines. The treatment induced protoporphyrine IX accumulation involved in melanogenesis since it promotes stability of cAMP. Finally, the Mek 1/2 inhibitor U0126 significantly potentiated growth inhibition of B16 cells triggered by 5,7-dimethoxycoumarin, suggesting that down-regulation of Raf/Mek/Erk pathway sensitizes melanoma cells to 5,7-dimethoxycoumarin treatment.

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“…Beside the compounds derived from the approved photosensitizers, texaphirins [54], etiopurpurins [55] and pheophorbides [56] are also in clinical trials.…”

Section: Pdt In Clinical Practicementioning

confidence: 99%

A look at clinical applications and developments of photodynamic therapy

et al. 2008

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The battle against cancer is so important that all possible weapons must be considered. Photodynamic therapy (PDT) is a therapeutic approach which has proved its capacity to give many excellent results, but it is having some difficulty in being imposed. The simplicity of the mechanism of action of this technique has been compromised by the multidisciplinary approach required for its implementation, which makes its adoption for more general use by health professionals difficult. This review aims to give a perspective of the performance of current approved PDT drugs, and their clinical applications against cancer.Basic investigation in PDT, particularly in the design of new sensitizers, is still ongoing, and needs to be further exploited. Emergent and diversified solutions with excellent results in pre-clinical phases are described to raise the multidisciplinary interest required to boost the clinical use of PDT.

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Specificity of photosensitizer accumulation in undifferentiated versus differentiated colon carcinoma cells

Cited by 25 publications

References 17 publications

Chrysin-induced apoptosis is mediated through p38 and Bax activation in B16-F1 and A375 melanoma cells

Chrysin-induced apoptosis is mediated through p38 and Bax activation in B16-F1 and A375 melanoma cells

Inhibition of Mek 1/2 kinase activity and stimulation of melanogenesis by 5,7-dimethoxycoumarin treatment of melanoma cells

A look at clinical applications and developments of photodynamic therapy

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