Abstract
Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine involved in the carcinogenesis of many cancer types. Here, we review the published experimental and clinical data for MIF and its involvement in melanoma. All reported data show that MIF is overexpressed in melanoma cells, especially in case of metastatic disease. Clinical studies also indicate that high MIF expression is positively associated with aggressiveness of the disease. Some data also highlight the implication of MIF in angiogenesis, immunity and metastasis in melanoma cell lines, as well as the availability of different therapeutic options targeting MIF for the treatment of metastatic melanoma. Indeed, the main problem in metastatic melanoma is the lack of long-term effective treatment. This is linked to the capacity of melanoma cells to mutate very quickly and/or activate alternative signaling pathways. Thus, MIF targeting therapies could provide a new effective way of treating melanoma. Moreover, cell sensitivity to MIF depletion does not correlate with the BRAF mutational status. Regarding the fact that many melanoma patients carry a BRAF mutation, and that they develop resistance to BRAF inhibitors, this observation is very interesting as MIF inhibitors could be used to treat many patients in relapse after treatment with an inhibitor of the mutant BRAF protein.
Highlights
Melanoma is the most common and deadliest form of skin cancer
In the past few years, migration inhibitory factor (MIF) has been largely studied in oncology for its major role in many tumorigenic pathways, such as angiogenesis, metastasis, and, most of all, immunity
Our review highlights that MIF could be a target of choice in metastatic melanoma treatment, where there is a significant lack of therapies after the development of resistance to targeted and immunotherapies
Summary
Melanoma is the most common and deadliest form of skin cancer. This type of tumor is affecting an increasing number of young adults. Melanoma represents the first form of cancer among people aged 25 to 29 [1]. This disease is difficult to treat, especially when diagnosed at a late stage. The major challenge with these kinds of inhibitors is that melanoma cells possess an hypermutable genome and many alternative signaling pathways, leading to resistances to such therapies [3], further supporting the use of a combination of treatments [1]
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