Ultraviolet A exposure alters adhesive properties of mouse melanoma cells

Pastila, Riikka; Leszczyński, D

doi:10.1111/j.1600-0781.2005.00166.x

Cited by 11 publications

(15 citation statements)

References 34 publications

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“…injection is a metastasis-like event resembling the hematogenous metastasis of melanoma and gives an indication of their metastatic potential, as shown by Fidler [17,18]. We have also demonstrated that UVA exposure causes the increase in the adhesiveness melanoma cells to endothelium in vitro , what is accompanied by changes in the expression of the cell surface adhesion molecules [19]. Thus, we proposed that the UVA-derived changes in the expression of adhesion molecules could be, at least in part, responsible for the in vivo observed increase of pulmonary tumor colonies in mice.…”

Section: Introductionmentioning

confidence: 74%

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In vivo UVA irradiation of mouse is more efficient in promoting pulmonary melanoma metastasis than in vitro

Pastila

Heinävaara

Ylianttila

et al. 2011

Cancer Cell International

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BackgroundWe have previously shown in vitro that UVA increases the adhesiveness of mouse B16-F1 melanoma cells to endothelium.We have also shown in vivo that UVA exposure of C57BL/6 mice, i.v. injected with B16-F1 cells, increases formation of pulmonary colonies of melanoma. The aim of the present animal study was to confirm the previously observed in vivo UVA effect and to determine whether in vitro UVA-exposure of melanoma cells, prior the i.v. injection, will have an enhancing effect on the pulmonary colonization capacity of melanoma cells. As a second aim, UVA-derived immunosuppression was determined.MethodsMice were i.v. injected with B16-F1 cells into the tail vein and then immediately exposed to UVA. Alternatively, to study the effect of UVA-induced adhesiveness on the colonization capacity of B16-F1 melanoma, cells were in vitro exposed prior to i.v. injection. Fourteen days after injection, lungs were collected and the number of pulmonary nodules was determined under dissecting microscope. The UVA-derived immunosuppression was measured by standard contact hypersensitivity assay.Results and DiscussionObtained results have confirmed that mice, i.v. injected with B16-F1 cells and thereafter exposed to UVA, developed 4-times more of melanoma colonies in lungs as compared with the UVA non-exposed group (p < 0.01). The in vitro exposure of melanoma cells prior to their injection into mice, led only to induction of 1.5-times more of pulmonary tumor nodules, being however a statistically non-significant change. The obtained results postulate that the UVA-induced changes in the adhesive properties of melanoma cells do not alone account for the 4-fold increase in the pulmonary tumor formation. Instead, it suggests that some systemic effect in a mouse might be responsible for the increased metastasis formation. Indeed, UVA was found to induce moderate systemic immunosuppression, which effect might contribute to the UVA-induced melanoma metastasis in mice lungs.

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Section: Introductionmentioning

confidence: 74%

“…UVB radiation was filtered out with a 5 mm thick glass filter. The spectral irradiances were measured with a temperature stabilized Bentham DM150 (Bentham Instruments Ltd., Berkshire, England) double-monochromator spectroradiometer at 0.5 nm intervals from 250 nm to 400 nm as described previously [16,19]. …”

Section: Methodsmentioning

confidence: 99%

In vivo UVA irradiation of mouse is more efficient in promoting pulmonary melanoma metastasis than in vitro

Pastila

Heinävaara

Ylianttila

et al. 2011

Cancer Cell International

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“…The four hour time-point was selected in order to give melanoma cells time to respond to UVA radiation in transcriptional level. Furthermore, 4-h time-point was also used in our preliminary in vitro set-up, where we have observed alterations in the adhesive properties of the melanoma cells 4 hours after the end of irradiation [14]. …”

Section: Discussionmentioning

confidence: 99%

“…The irradiances of the UVA source were measured as described previously [14,28]. Briefly, the irradiances were determined with a temperature- and wavelength-controlled Optronic 742 double-holographic grating spectroradiometer having a Teflon diffuser as input optics at 1 nm intervals from 250 to 400 nm.…”

Section: Methodsmentioning

confidence: 99%

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Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

Pastila

Leszczyński

2007

Cancer Cell Int

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BackgroundWe have previously shown that ultraviolet-A (UVA) radiation enhances metastatic lung colonization capacity of B16-F1 melanoma cells. The aim of this study was to examine changes in expression profile of genes in mouse melanoma B16-F1 cells exposed to UVA radiation.ResultsB16-F1 melanoma cells were exposed to a single UVA radiation dose of 8 J/cm2 and mRNA was isolated 4 h after the end of UVA exposure. Atlas™ Mouse Cancer 1.2 cDNA expression arrays were used for the large-scale screening to identify the genes involved in the regulation of carcinogenesis, tumor progression and metastasis. Physiologically relevant UVA dose induced differential expression in 9 genes in the UVA exposed melanoma cells as compared to the unexposed control cells. The expression of seven genes out of nine was upregulated (HSC70, HSP86, α-B-crystallin, GST mu2, Oxidative stress induced protein OSI, VEGF, cyclin G), whereas the expression of two genes was down-regulated (G-actin, non-muscle cofilin). The gene expression of cyclin G was mostly affected by UVA radiation, increasing by 4.85-folds 4 hour after exposure. The analysis of cyclin G protein expression revealed 1.36-fold increase at the 6 hour time point after UVA exposure. Cell cycle arrest in G2/M phase, which is known to be regulated by cyclin G, occurred at 4-h hour time-point, peaking 8 hours after the end of UVA irradiation, suggesting that cyclin G might play a role in the cell cycle arrest.ConclusionOur results suggest that UVA radiation-induces changes in the expression of several genes. Some of these changes, e.g. in expression of cyclin G, possibly might affect cell physiology (cell cycle arrest).

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The Role of Classical and Novel Forms of Vitamin D in the Pathogenesis and Progression of Nonmelanoma Skin Cancers

Słomiński

Brożyna

Żmijewski

et al. 2020

Advances in Experimental Medicine and Biology

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Nonmelanoma skin cancers including basal and squamous cell carcinomas (SCC and BCC) represent a significant clinical problem due to their relatively high incidence, imposing an economic burden to healthcare systems around the world. It is accepted that ultraviolet radiation (UVR: λ = 290-400 nm) plays a crucial role in the initiation and promotion of BCC and SCC with UVB (λ = 290-320 nm) having a central role in this process. On the other hand, UVB is required for vitamin D3 (D3) production in the skin, which supplies >90% of the body's requirement for this prohormone. Prolonged exposure to UVB can also generate tachysterol and lumisterol. Vitamin D3 itself and its canonical ( 1,25(OH)2D3) and noncanonical (CYP11A1-intitated) D3 hydroxyderivatives show photoprotective functions in the skin. These include regulation of keratinocyte proliferation and differentiation, induction of anti-oxidative responses, inhibition of DNA damage and induction of DNA repair mechanisms, and anti-inflammatory activities. Studies in animals have demonstrated that D3 hydroxyderivatives can attenuate UVB or chemically induced epidermal cancerogenesis and inhibit growth of SCC and BCC. Genomic and nongenomic mechanisms of action have been suggested. In addition, vitamin D3 itself inhibits hedgehog signaling pathways which have been implicated in many cancers. Silencing of the vitamin D receptor leads to increased propensity to develop UVB or chemically induced epidermal cancers. Other targets for vitamin D compounds include 1,25D3-MARRS, retinoic orphan receptors α and γ, aryl hydrocarbon receptor, and Wnt signaling. Most recently, photoprotective effects of lumisterol hydroxyderivatives have been identified. Clinical trials demonstrated a beneficial role of vitamin D compounds in the treatment of actinic keratosis. In summary, recent advances in vitamin D biology and pharmacology open new exciting opportunities in chemoprevention and treatment of skin cancers.

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Ultraviolet A exposure alters adhesive properties of mouse melanoma cells

Cited by 11 publications

References 34 publications

In vivo UVA irradiation of mouse is more efficient in promoting pulmonary melanoma metastasis than in vitro

In vivo UVA irradiation of mouse is more efficient in promoting pulmonary melanoma metastasis than in vitro

Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells

The Role of Classical and Novel Forms of Vitamin D in the Pathogenesis and Progression of Nonmelanoma Skin Cancers

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