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Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression
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Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression
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Journal Article
Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression
2015
Overview
Background
Accumulating evidence suggests that some long noncoding RNAs (lncRNAs) are involved in certain diseases, such as cancer. The lncRNA,
CCDC26
, is related to childhood acute myeloid leukemia (AML) because its copy number is altered in AML patients.
Results
We found that
CCDC26
transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. To examine the function of
CCDC26
, gene knockdown (KD) was performed using short hairpin RNAs (shRNAs), and four KD clones, in which
CCDC26
expression was suppressed to 1% of its normal level, were isolated. This down-regulation included suppression of
CCDC26
intron-containing transcripts (the
CCDC26
precursor mRNA), indicating that transcriptional gene suppression (TGS), not post-transcriptional suppression, was occurring. The shRNA targeting one of the two
CCDC26
splice variants also suppressed the other splice variant, which is further evidence for TGS. Growth rates of KD clones were reduced compared with non-KD control cells in media containing normal or high serum concentrations. In contrast, enhanced growth rates in media containing much lower serum concentrations and increased survival periods after serum withdrawal were observed for KD clones. DNA microarray and quantitative polymerase chain reaction screening for differentially expressed genes between KD clones and non-KD control cells revealed significant up-regulation of the tyrosine kinase receptor,
KIT
, hyperactive mutations of which are often found in AML. Treatment of KD clones with ISCK03, a KIT-specific inhibitor, eliminated the increased survival of KD clones in the absence of serum.
Conclusions
We suggest that
CCDC26
controls growth of myeloid leukemia cells through regulation of
KIT
expression. A KIT inhibitor might be an effective treatment against the forms of AML in which
CCDC26
is altered.
Publisher
BioMed Central,BioMed Central Ltd
Subject
/ Biomedical and Life Sciences
/ Cell Proliferation - drug effects
/ Cell Survival - drug effects
/ Gene Expression Regulation, Leukemic - drug effects
/ Gene Silencing - drug effects
/ Genes
/ Genetic Vectors - metabolism
/ Growth
/ Humans
/ Leukemia, Myeloid, Acute - genetics
/ Leukemia, Myeloid, Acute - pathology
/ Oncology
/ Protein Kinase Inhibitors - pharmacology
/ Proto-Oncogene Proteins c-kit - antagonists & inhibitors
/ Proto-Oncogene Proteins c-kit - genetics
/ Proto-Oncogene Proteins c-kit - metabolism
/ RNA, Long Noncoding - genetics
/ RNA, Long Noncoding - metabolism
/ RNA, Small Interfering - metabolism
/ Serum
/ Tyrosine
