The metastatic transformation of melanocytes is associated with altered expression of adhesion molecules, including alpha(v)beta(3) and alpha(3)beta(1) integrins. Integrin alpha(v)beta(3) is a primary vitronectin (VN) receptor, while both integrin types take part in adhesion to VN when they are in complex with uPAR. Although their role in melanoma cell interaction with VN is of great interest, the influence of N-oligosaccharides attached to these glycoproteins is still unappreciated. The present study assesses the role of alpha(v)beta(3) and alpha(3)beta(1) integrins and the influence of their glycosylation status on WM9 and WM239 metastatic melanoma cell interactions with VN. Cell adhesion to and migration on VN were selected as the studied cell behaviour parameters. Function-blocking antibodies and swainsonine (SW) treatment were used in these tests. Both cell lines interacted with VN in an integrin-mediated but cell-line-specific manner. In WM9 cells, migration was not completely inhibited by antibodies against alpha(3)beta(1) or alpha(v)beta(3) integrins, suggesting the participation of other VN receptors. In both cell lines in coprecipitation test the formation of an integrins/uPAR complex was shown. In the presence of SW formation of the complex did not occur, suggesting the participation of glycosylation in this process. Additionally, the adhesion properties of WM9 cells were changed after SW treatment. Our results suggest that in these two metastatic cell lines integrin-linked N-oligosaccharides influence the VN adhesion receptor activity and function.

The short wavelength, i.e., blue light, is crucial for non-image forming effects such as entrainment of the circadian system in humans. Moreover, many studies showed that blue light enhances alertness and performance in cognitive tasks. However, most scientific reports in this topic are based on experiments using short exposure to blue or blue-enriched light, and only a few focused on the effects of its reduced transmittance, especially in longer periods. The latter could potentially give insight into understanding if age-related sleep problems and cognitive decline are related to less amount of blue light reaching the retina, as the eyes' lenses yellow with age. In this study, we investigated the effects of prolonged blocking of blue light on cognitive functioning, in particular-sustained attention and visuospatial working memory, as well as on sleep, and melatonin and cortisol levels. A group of young, healthy participants was randomly allocated to either blue light blocking or control group. Depending on the group, participants wore amber contact lenses, reducing the transmittance of blue light by ∼90% or regular contact lenses for a period of 4 weeks. No changes were observed for measurements related to sleep and sleep-wake rhythm. Dim light melatonin onset, evening levels of melatonin, and morning cortisol answer did not show any significant alterations during blue light (BL) blockade. The significant effects were revealed both for sustained attention and visuospatial memory, i.e., the longer blocking the blue light lasted, the greater decrease in performance observed. Additionally, the followup session conducted ∼1 week after taking off the blue-blocking lenses revealed that in case of sustained attention, this detrimental effect of blocking BL is fully reversible. Our findings provide evidence that prolonged reduction of BL exposure directly affects human cognitive functioning regardless of circadian rhythmicity.

Melanoma is the most aggressive of all skin cancers and is exceptionally resistant to therapies. During melanoma progression, cancer cells reprogram their proliferation and survival pathways and achieve resistance to treatment-induced apoptosis. Galectin-3 (gal-3) is a member of the lectin family and is involved in such biological processes as cell adhesion, growth and differentiation, the cell cycle, and apoptosis. Gal-3 also plays an important role in tumor development and metastasis. The relationship between gal-3 expression and these processes is specific to the tumor type and the stage of cancer progression. The biological functions of gal-3 depend on its localization in the cell. In the present study, human metastatic melanoma A-375 cells, characterized by weak endogenous expression of gal-3, were transfected with gal-3 cDNA and cisplatin-induced apoptosis was measured. Data from AnnexinV and mitochondrial membrane potential analysis revealed that gal-3 did not protect the A-375 melanoma cells against cisplatin. This result probably is associated with its nuclear localization in the cells.

The number of overweight and obese people is increasing at an alarming rate, especially in the developed and developing countries. Obesity is a major risk factor for diabetes, cardiovascular disease, and cancer, and in consequence for premature death. The development of obesity results from the interplay of both genetic and environmental factors, which include sedentary life style and abnormal eating habits. In the past few years a number of events accompanying obesity, affecting expression of genes which are not directly connected with the DNA base sequence (e.g. epigenetic changes), have been described. Epigenetic processes include DNA methylation, histone modifications such as acetylation, methylation, phosphorylation, ubiquitination, and sumoylation, as well as non-coding micro-RNA (miRNA) synthesis. In this review, the known changes in the profile of DNA methylation as a factor affecting obesity and its complications are described.