Abstract
RUNX2, a master osteogenic transcript ion factor, is overexpressed in several cancer cells; in melanoma it promotes cells migration and invasion as well as neoangiogenesis. The annual mortality rates related to metastatic melanoma are high and novel agents are needed to improve melanoma patients’ survival. It has been shown that lectins specifically target malignant cells since they present the Thomsen–Friedenreich antigen. This disaccharide is hidden in normal cells, while it allows selective lectins binding in transformed cells. Recently, an edible lectin named BEL β-trefoil has been obtained from the wild mushroom Boletus edulis. Our previous study showed BEL β-trefoil effects on transcription factor RUNX2 downregulation as well as on the migration ability in melanoma cells treated in vitro. Therefore, to better understand the role of this lectin, we investigated the BEL β-trefoil effects in a zebrafish in vivo model, transplanted with human melanoma cells expressing RUNX2. Our data showed that BEL β-trefoil is able to spread in the tissues and to reduce the formation of metastases in melanoma xenotransplanted zebrafish. In conclusion, BEL β-trefoil can be considered an effective biomolecule to counteract melanoma disease.
Highlights
The incidence of malignant melanoma, a dangerous type of cancer, has been increasing in recent years [1]
It has been demonstrated that RUNX2, an important osteogenic transcription factor which is overexpressed in thyroid cancer [2], promotes melanoma cells’
We have investigated the effects of Boletus edulis lectin (BEL) β-trefoil against RUNX2- expressing melanoma cells in vivo by using a xenotransplant model of zebrafish
Summary
The incidence of malignant melanoma, a dangerous type of cancer, has been increasing in recent years [1]. It is a highly metastatic tumour generally resistant to apoptosis as well as to chemotherapeutic treatments and local tumour surgery, the standard treatment used. Recent data have suggested that several types of melanoma arise from modifications in genes controlling metabolism, which promote cell proliferation and tumour growth. Genomic sequencing of melanoma cells revealed that this cancer is very heterogeneous: point mutations, deletions and translocations characterize individual tumours [1]. It has been demonstrated that RUNX2, an important osteogenic transcription factor which is overexpressed in thyroid cancer [2], promotes melanoma cells’
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