Background: We have examined whether ultraviolet A (UVA) irradiation could alter adhesive properties of melanoma cells. As an experimental in vitro model, we have used C57BL/6 mouse-derived B16- F1 and B16-F10 melanoma cell lines and the syngeneic MS-1 endothelial cell line.
Method/result: The melanoma cells were exposed to different doses of UVA irradiation. We have determined that a single dose of UVA at 8 and 12 J/cm(2) causes an 88% (P<0.001) and a 32% (P<0.05) increase in B16-F1 melanoma cell adhesiveness to the non-irradiated endothelial monolayer, respectively. The peak of the response was 24 h after the irradiation. The UVA dose of 8 J/cm(2) delivered in four doses separated by 1 h intervals (4 x 2 J/cm(2)) had led to a caused 149% (P<0.001) increase of B16-F1 melanoma adhesiveness already at 1 h after the last dose of UVA. Besides the induction of increase in the melanoma-endothelial cell adhesion, UVA exposure has induced a rapid decline (1 h after exposure) in homotypic melanoma-melanoma cell adhesion (clustering). The clustering decline of B16-F1 cells with a single dose of UVA at 8 J/cm(2) was by 61% (P<0.05) and by 35% (P<0.05) with 4 x 2 J/cm(2). Pilot experiments have shown that the changes of the adhesive properties of melanoma cells were accompanied by an increase in N-cadherin expression and a decline in E-cadherin expression. Such a change in cadherin expression profile has been shown to be an indicator of the increased metastatic potential.
Conclusion: Our results suggest that UVA radiation appears to alter the adhesive properties of melanoma cells in vitro, by diminishing the melanoma-melanoma adhesion and by increasing melanoma adhesion to the endothelium. This suggests that UVA exposure might increase the metastatic capability of the melanoma cells.
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http://dx.doi.org/10.1111/j.1600-0781.2005.00166.x | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Pharmacy, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Pulmonary metastasis represents one of the most prevalent forms of metastasis in advanced melanoma, with mortality rates reaching 70%. Current treatments including chemotherapy, targeted therapy, and immunotherapy frequently exhibit limited efficacy or present high costs. To address these clinical needs, this study presents a biomimetic drug delivery system (Ce6-pTP-CsA) utilizing cryoshocked adipocytes (CsA) encapsulating the prodrug triptolide palmitate (pTP) and the photosensitizer Ce6, exploiting the characteristic of tumor cells to recruit and lipolyze adipocytes for energy.
View Article and Find Full Text PDFCancer Res Commun
January 2025
University of British Columbia, Vancouver, BC, Canada.
NF1 encodes the multifunctional tumour suppressor protein, neurofibromin, which is best known for its causative role in Neurofibromatosis type 1 and in regulating MAPK signaling. Neurofibromin, in a context-specific manner, is involved in various tumorigenic processes, including those in melanocytes. This study investigated whether NF1 loss can collaborate with oncogenic GNAQ to promote melanoma in the dermis or eyes, where the G alpha q pathway is almost always activated.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
The Key Laboratory of Molecular Pharmacology, Liaocheng People's Hospital, Liaocheng, Shandong, People's Republic of China.
Background: Melanoma is a highly lethal form of skin cancer, and effective treatment remains a significant challenge. SPP86 is a novel potential therapeutic drug. Nonetheless, the specific influence of SPP86 on autophagy, particularly its mechanisms in the context of DNA damage and apoptosis in human melanoma cells, remains inadequately understood.
View Article and Find Full Text PDFCells under high confinement form highly polarized hydrostatic pressure-driven, stable leader blebs that enable efficient migration in low adhesion, environments. Here we investigated the basis of the polarized bleb morphology of metastatic melanoma cells migrating in non-adhesive confinement. Using high-resolution time-lapse imaging and specific molecular perturbations, we found that EGF signaling via PI3K stabilizes and maintains a polarized leader bleb.
View Article and Find Full Text PDFMater Today Bio
February 2025
Terasaki Institute for Biomedical Innovation (TIBI), Los Angeles, CA, 90024, USA.
Skin-on-a-chip models provide physiologically relevant platforms for studying diseases and drug evaluation, replicating the native skin structures and functions more accurately than traditional 2D or simple 3D cultures. However, challenges remain in creating models suitable for microneedling applications and monitoring, as well as developing skin cancer models for analysis and targeted therapy. Here, we developed a human skin/skin cancer-on-a-chip platform within a microfluidic device using bioprinting/bioengineering techniques.
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