Bone Morphogenic Protein Signaling and Melanoma.

Opinion Statement: Malignant melanoma is a deadly form of skin cancer caused by neoplastic transformation of melanocytic cells. Despite recent progress in melanoma therapy, by inhibition of activated oncogenes or immunotherapy, survival rate for metastatic melanoma patients remains low. The remarkab...

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Publicado en:Current Treatment Options in Oncology Vol. 22; no. 6; pp. 1 - 13
Autor principal: Kraj, Piotr
Formato: review Journal Article
Publicado: Springer Nature Jun2021
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Springer Nature
      place: New York, New York
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        atl: Bone Morphogenic Protein Signaling and Melanoma.
      aug:
        au: Kraj, Piotr
        affil: Department of Biological Sciences, Old Dominion University, Mills Godwin Building, 5115 Hampton Blvd, 23529, Norfolk, VA, USA
      sug:
        subj:
          Bone Morphogenetic Proteins Physiology
          Melanoma Etiology
          Skin Neoplasms Etiology
          Skin Neoplasms Pathology
          Cell Transformation, Neoplastic
          Melanoma Pathology
          Signal Transduction Physiology
          Scales
      ab: Opinion Statement: Malignant melanoma is a deadly form of skin cancer caused by neoplastic transformation of melanocytic cells. Despite recent progress in melanoma therapy, by inhibition of activated oncogenes or immunotherapy, survival rate for metastatic melanoma patients remains low. The remarkable phenotypic plasticity of melanoma cells allows for rapid development of invasive properties and metastatic tumors, the main cause of mortality in melanoma patients. Phenotypic and molecular analyses of developing tumors revealed that epithelial-mesenchymal transition (EMT), a cellular and molecular mechanism, controls transition from mature melanocyte to less differentiated melanocyte lineage progenitor cells forming melanoma tumors. This transition is facilitated by persistence of transcriptional regulatory circuit characteristic of embryonic stage in mature melanocytes. Switching of the developmental program of mature melanocyte to EMT is induced by accumulated mutations, especially targeting BRAF, N-RAS, or MEK1/2 signaling pathways, and further promoted by dynamic stimuli from local environment including hypoxia, interactions with extracellular matrix and growth factors or cytokines. Recent reports demonstrate that signaling mediated by transforming growth factor-β (TGF-β) and bone morphogenic proteins (BMPs) play critical roles in inducing EMT by controlling expression of critical transcription factors. BMPs are essential modulators of differentiation, proliferation, apoptosis, invasiveness, and metastases in developing melanoma tumors. They control transcription and epigenetic landscape of melanoma cells. Better understanding of the role of BMPs may lead to new strategies to control EMT processes in melanocyte cell lineage and to achieve clinical benefits for the patients.
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        review
        Journal Article
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    language: English
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