Linking MLL and the HGF-MET signaling pathway in liver cancer.
Level V
Where this comes from
- Record sourced from PubMed, PMID 23934122.
- Also identified by DOI 10.1172/JCI70235 and PMC identifier 3696572.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
Mixed-lineage leukemia (MLL; also known as myeloid/lymphoid), the human homolog of trithorax in Drosophila, is a transcriptional coactivator that plays an essential role during early development and hematopoiesis. Furthermore, MLL is critically involved in the epigenetic regulation of cell cycle, senescence, DNA damage, and stem cell self-renewal. Chromosomal aberrations of MLL in acute leukemias are well documented, but the role of this gene in solid malignancies remains unclear. In this issue of the JCI, Takeda et al. describe a novel epigenetic link between MLL and the HGF-MET signaling pathway conferring invasive and metastatic properties to hepatocellular carcinoma cells.
Medical subject headings
- Carcinoma, Hepatocellular
- Hepatocyte Growth Factor
- Liver Neoplasms, Experimental
- Myeloid-Lymphoid Leukemia Protein
- Proto-Oncogene Protein c-ets-2
- Proto-Oncogene Proteins c-met