LPS was applied as a dose gradient (10 U/ml equals 0.25 ng/ml). The concentration of the attracting agent FBS in the lower section of the migration chamber was 7.3–7.5%. Migration was carried out for 4.5–5 h at 37°C in CO2. The cells were stained and counted under light microscopy on the whole membrane. The mean number of cells per membrane (bars) and SD (lines) are presented. Discussion The most

important question of this study was the general effect of the bacteriophage preparations on melanoma’s migration activity, mostly because of the perspective of developing bacteriophage therapy. The migration of human and mouse melanoma can be inhibited by the purified T4 and HAP1 bacteriophage preparations with no stimulative action, which is plainly an advantageous

effect. A response of melanoma cells to LPS (within the investigated range) was not observed and the differences from those of the check details bacteriophage preparations were marked, so the antimigration activity of the studied preparations cannot be attributed to LPS. It should be pointed out that the LPS content in the purified phage preparation was minimal; in this study the final concentration was 0.25 ng/ml (10 U/ml by the chromogenic Limulus amoebocyte lysate assay). The high variability of the assay hindered analysis of the observations. The more general assay with matrigel was also much more variable and it ascertained Liproxstatin1 only an inhibitory effect of HAP1 on Hs294T migration. In the fibronectin assay, significant inhibition

was observed both for the mouse (T4 and HAP1) and human (T4) melanoma. This is in line with the hypothesis on the RGD-engaging mechanism of changes in cell migration [15] as cell adhesion to the ECM is mediated by fibronectin’s RGD sequences. Integrins alpha(v)beta(3), alpha(IIb)beta(3), and alpha(5)beta(1) mediate cancer cell motility and adhesion and are susceptible to the activity of RGD homologues. They are known to promote metastasis and malignancy and to be highly expressed in melanoma cells (in contrast to normal melanocytes). Alpha(v)beta(3) and beta(1)-integrins are highly expressed at the leading edge of invasive explants. They also regulate MMPs functions that are critical for the invasive properties of tumour cells as they degrade ECM components [18, 19]. The overall mechanism of melanoma motility Molecular motor is obviously complex and engages a wider range of surface particles. Other factors strongly associated with melanoma development and progression that also play roles in melanoma adhesion and motility are melanoma cell adhesion molecule (Mel-CAM, MUC18, CD146), L1 cell adhesion molecule (L1-CAM, CD171), activated leukocyte cell adhesion molecule (ALCAM, CD166), vascular cell adhesion molecule 1 (VCAM-1, CD106), intracellular cell adhesion molecule 1 (ICAM-1, CD54), and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1, CD66a) [19].