Download miRNA candidate

Table 4. Selected relevant mRNA targets for novel miRNA candidatesa.
miRNA
candidate
M-17
M-17
Target Gene
Symbol
HES3
EPHA10
Location
Score
1p36.31
1p34.3
1359
1049
PRDM16
1p36.32
859
M-64
PR domain-containing protein 16: PR (positive regulatory domain I binding
factor 1 and retinoblastoma-interacting zinc finger protein) domain
hairy/enhancer of split, drosophila, homolog 2
HES2
1p36.31
674
M-64
wingless-type mmtv integration site family, member 3a
WNT3A
1q42.13
584
M-64
Sry-Box 11
SOX11
2p25.2
539
M-64
plexin A1
PLXNA1
3q21.2
498
M-84
chromodomain helicase DNA-binding protein 5
CHD5
1p36.31
176
M-84
glutathione s-transferase, Mu-1
GSTM1
1p13.3
148
M-84
regulator of G protein signaling 2
RGS2
1q31.2
131
M-94
PR domain-containing protein 16
PRDM16
1p36.32
1644
M-94
chromodomain helicase DNA-binding protein 5
CHD5
1p36.31
1500
M-94
hairy/enhancer of split, drosophila, homolog of, 3
HES3
1p36.31
1467
M-94
runt-related transcription factor 3
RUNX3
1p36.11
1319
M-94
SRY-box 13
SOX13
1q32.1
1272
M-94
wingless-type mmtv integration site family, member 3A
WNT3A
1q42.13
1239
NM-84
PR domain-containing protein 16
PRDM16
1p36.32
1277
NM-84
chromodomain helicase DNA-binding protein 5
CHD5
1p36.31
1015
NM-84
hairy/enhancer of split, drosophila, homolog of, 3
HES3
1p36.31
1003
NM-84
ephrin receptor EphB2
EPHB2
1p36.12
942
M-64
a
Target Gene Name
hairy/enhancer of split, drosophila, homolog 3
ephrin receptor (receptor tyrosine kinases; rtks)
et al.
(2002) showed
thatidentified
beta-catenin (116806)
and TCF
Predicted Batlle
target
mRNAs
were
through
the (see
miRanda algorithm
TCF7L2; 602228) inversely control the expression of the EphB2/EphB3
(601839) receptors and their ligand, ephrin B1 (EFNB1; 300035), in
colorectal cancer and along the crypt-villus axis. Disruption of EphB2 and
EphB3 genes revealed that their gene products restrict cell intermingling and
allocate cell populations within the intestinal epithelium. In EphB2/EphB3
null mice, the proliferative and differentiated populations intermingled. In
adult EphB3 -/- mice, Paneth cells did not follow their downward migratory
path, but scattered along crypt and villus. The authors concluded that, in the
intestinal epithelium, beta-catenin and TCF couple proliferation and
differentiation to the sorting of cell populations through the EphB/ephrin B
system. Huusko et al. (2004) combined emetine inhibition of nonsensemediated decay (NMD) and microarray analysis with comparative genomic
hybridization (CGH) to screen prostate cancer-derived cell lines for
transcripts that undergo NMD and are transcribed from genes with deletions
on both alleles. This way they could identify genes with inactivation of the 1
allele by a nonsense mutation and loss of the outer allele through deletion.
They identified previously unknown mutations in the EPHB2 gene. The DU
145 prostate cancer cell line, originating from a brain metastasis, was found
to carry a truncating mutation of EPHB2 (600997.0001) and a deletion of the
remaining allele. Additional frameshift, splice site, missense, and nonsense
mutations were present in clinical prostate cancer samples. Transfection of
DU 145 cells, which lack functional EPHB2, with wildtype EPHB2
suppressed clonogenic growth. These studies indicated that EPHB2 may
have an essential role in cell migration and maintenance of normal tissue
architecture and that mutational inactivation of the EPHB2 gene may be
important in the progression and metastasis of prostate cancer. Mercola and
Welsh (2004) reviewed the combination of methods, emetine suppression of
NMD and microarray analysis with CGH, for identifying disease-gene
associations. As many as one-third of inherited disorders are caused by
mutations that disrupt reading frames.