A long noncoding RNA (lncRNA), which might have an impact on tyrosine kinase-targeted leukemia therapy, has been found to be expressed in a leukemia cell line. The function of this lncRNA (CCDC26) is not fully understood; however, researchers at Hiroshima University have revealed the mechanisms by which CCDC26 lncRNA controls expression of the receptor tyrosine kinase KIT. The results provide new insights into leukemia recurrence and may help to develop new leukemia therapies. Recent transcriptomic studies have revealed the existence of numerous RNAs that are relatively long, but not translated into proteins. Some of such lncRNAs are suggested to regulate the expression of other genes. Mutations or imbalances in the noncoding RNA repertoire within the body can likely cause a variety of diseases, including cancer. However, the molecular functions of lncRNAs remain to be fully elucidated. Dr. Tetsuo Hirano from the Graduate School of Integrated Arts and Science at Hiroshima University found that knockdown of the CCDC26 gene in cells results in significant up-regulation of the KIT gene, hyperactive mutations of which are often found in acute myeloid leukemia. Dr. Hirano and his collaborators at the School of Medicine in Juntendo University showed that CCDC26 transcript levels are high in the nuclear fraction of human myeloid leukemia cell lines. They also found that CCDC26 knockdown induces suppression of CCDC26 intron-containing transcripts, indicating transcriptional gene suppression. Leukemia cells in which CCDC26 was knocked down showed enhanced survival periods after serum withdrawal. A KIT-specific inhibitor reversed this increased survival of the cells.
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