Journal
GENES
Volume 11, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/genes11111342
Keywords
BRAF; MAPK; ERK; oncogene; mutations; transcription factors; cancer
Categories
Funding
- National Science Centre, Poland [2017/25/N/NZ5/01885]
- Platform Project for Supporting Drug Discovery and Life Science Research (BINDS) from Japan Agency for Medical Research and Development (AMED) [JP19am0101106j0003, 1538]
- RIKEN Pioneering research project, Dynamic Structural Biology
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Gene mutations can induce cellular alteration and malignant transformation. Development of many types of cancer is associated with mutations in the B-raf proto-oncogene (BRAF) gene. The encoded protein is a component of the mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway, transmitting information from the outside to the cell nucleus. The main function of the MAPK/ERK pathway is to regulate cell growth, migration, and proliferation. The most common mutations in the BRAF gene encode the V600E mutant (class I), which causes continuous activation and signal transduction, regardless of external stimulus. Consequently, cell proliferation and invasion are enhanced in cancer patients with such mutations. The V600E mutation has been linked to melanoma, colorectal cancer, multiple myeloma, and other types of cancers. Importantly, emerging evidence has recently indicated that new types of mutations (classes II and III) also play a paramount role in the development of cancer. In this minireview, we discuss the influence of various BRAF mutations in cancer, including aberrant transcriptional gene regulation in the affected tissues.
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