sort by

15 publications mentioning hsa-mir-939

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-939. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 350
c real-time RT-PCR analysis showed that overexpression of miR-939 significantly suppressed SLC34A2 mRNA expression level of SLC34A2 of GC cells, while inhibition of miR-939 led to a noticeable increase in SLC34A2 mRNA expression level of GC cell. [score:11]
As shown in Fig.   4c, d, the expression levels of SLC34A2 mRNA and protein were significantly decreased following the ectopic expression of miR-939; In contrast, the inhibition of miR-939 led to an increase in the expression of SLC34A2 at both the mRNA and protein level. [score:9]
In addition, we identified that miR-939 exerts its tumor-suppressing role by targeting SLC34A2 via the inhibition of Raf-MEK-ERK signaling pathways. [score:7]
We confirmed that overexpression of miR-939 suppressed cellular migration and invasion, whereas miR-939 inhibition promoted migration and invasion in vitro (Fig.   3a-c). [score:7]
In the present study, we firstly examined the expression pattern of miR-939 in two independent cohorts of clinical GC samples: one cohort of 112 GC patients with stage I-III disease who underwent surgery followed by adjuvant chemotherapy; and another cohort of 110 GC patients with stage IV disease who received palliative chemotherapy. [score:7]
In addition, a series of in vitro and in vivo experiments demonstrated that miR-939 diminishes GC cell chemoresistance and metastatic ability by targeting SLC34A2 expression, with consequent inhibition of the Raf-MEK-ERK signaling pathway. [score:7]
In addition, our clinical data show that expression of SLC34A2 is inversely correlated with miR-939 expression, and that patients with high expression of SLC34A2 have a decreased survival rate. [score:7]
Consistently, overexpressing miR-939 mutation had no comprising effect on SLC34A2 mRNA and protein expression level (Fig.   4c, d). [score:6]
miR-939 enhances GC chemosensitivity and inhibits metastasis by directly targeting SLC34A2. [score:6]
Expression of miR-939 is downregulated in GC and closely related to clinical outcomes. [score:6]
Meanwhile, ectopically expressing miR-939 mutation had no inhibitory effect on the SLC34A2-3’UTR luciferase activity (Fig.   4b). [score:6]
We found obvious inhibition of RAF-MEK-ERK pathway upon miR-939 overexpression, whereas restoration of SLC34A2 attenuated this compromising effect (Fig.   5h). [score:5]
Further function study demonstrated that overexpression of miR-939 suppressed GC cell growth, and enhanced 5-fluorouracil -induced chemosensitivity by compromising cellular growth and inducing apoptosis in vitro and in vivo. [score:5]
Based on these findings, modulating miR-939 expression in GC appears to be an encouraging prototype therapeutic agent for cancer therapy, which might generate suppressing effect on GC chemotherapy resistance and distance metastasis. [score:5]
e high SLC34A2 IHC staining was observed in one GC sample with low miR-939 expression (upper panel); one GC sample with high miR-939 expression showed weak GNA13 IHC staining (lower panel). [score:5]
As lower expression of miR-939 was observed in patients with distant metastasis in GC, and distant metastasis often resulted in resistance to the conventional chemotherapy drugs, we sought to determine whether miR-939 has inhibition on GC metastasis. [score:5]
a concentration -dependent growth inhibition in response to 5-Fu in miR-939 -overexpressing, miR-939-silenced, and control GC cells. [score:5]
The miR-939 expression vector (HmiR0533-MR03), the control vector for miR-939 (CmiR0001-MR03), the coding sequences of SLC34A2 expression vector (EX-A3175-Lv105), and the control vector for SLC34A2 (EX-NEG-Lv105) were purchased from the GeneCopoeia Company (Guangzhou, China). [score:5]
a protein levels of overexpressed SLC34A2 lacking 3'UTR in miR-939 -overexpressing GC cells, as assessed by western blot. [score:5]
Also, exogenously expressed SLC34A2 compromised the inhibition of metastasis by miR-939 on GC cells (Fig.   5e-f). [score:5]
We found that the expression level of P-ERK was significantly decreased in cells with stable overexpression of miR-939 (Fig.   5g, lane 1, 2). [score:5]
a comparison miR-939 expression in six GC cell lines and non-transformed epithelial cell line, GES-1. b comparing differences in the expression levels of miR-939 between tumor and corresponding non-tumor tissues. [score:5]
f the expression of SLC34A2 was inversely correlated with the expression of miR-939 in 112 GC samples. [score:5]
Our data indicate that the restoration of SLC34A2 blocked the miR-939 overexpression -induced inhibition of cancer growth, cell proliferation, metastasis, and the induction of apoptosis. [score:5]
Right panel: the number of nodules was qualified on lungs of SCID mice (n = 6 per group) 4 weeks after tail vein injection of SGC-7901-scramble (left bars) and SGC7901-miR-939 cells (right bars) Using miRNA target prediction algorithms, we identified solute carrier family 34 member 2 (SLC34A2) as tentative target of miR-939 (Fig.   4a). [score:5]
d the predictive value of miR-939 expression regarding the chemotherapy response in 110 patients with advanced GC disease. [score:5]
g in GC cells with miR-939 overexpression, the expression levels of p-ERK (lane 2) were significantly decreased compared with the control (lane 1). [score:4]
Interestingly, while little is known about the role of miR-939 in human cancers, miR-939 is among a unique set of downregulated miRNAs in GC. [score:4]
h western blot analyses show that the expression of C-Raf and p-MEK was decreased in miR-939 -transfected cells, while increased after SLC34A2 overexpressed Previous studies have documented that PI3K/AKT and MAPK/ERK signaling pathway play crucial roles in development of chemoresistance and metastatic ability in human malignancies [14– 16], thus we investigated the roles of miR-939 in the activation of PI3K/AKT and MAPK/ERK pathway. [score:4]
Taken together, these findings demonstrated that SLC34A2 is an integral mediator of miR-939 function in GC cells via MEK-ERK MAPK pathway inhibition, which is known to be dysregulated in many cancers. [score:4]
As shown in Fig.   2e, we found that overexpression of miR-939 could significantly compromise GC tumor growth in vivo, and moreover, the combination of miR-939 and 5-Fu showed more significant inhibition of tumor growth, compared to either miR-939 or 5-Fu alone. [score:4]
Fig. 4SLC34A2 is the direct target of miR-939. [score:4]
The luciferase reporter assay indicated that overexpression of miR-939 significantly repressed the luciferase activity of SLC34A2-3’UTR, while inhibition of miR-939 increased the luciferase activity of SLC34A2-3’UTR. [score:4]
On the other hand, however, Ying reported upregulation of miR-939 in human ovarian cancer, which promoted cancer cell proliferation [22]. [score:4]
In this study, we found that miR-939 was indeed downregulated in GC tissues. [score:4]
Thus, the examination of miR-939 expression could be applied as an effective additional tool to optimize clinical decisions, enabling clinicians to identify those high-risk GC patients with increased risk of tumor recurrence and/or metastasis. [score:3]
Herein, it remains important to thoroughly understand the molecular mechanisms mediating the differential biologic effects and targets of miR-939 in GC and other cancer types. [score:3]
In summary, we provide comprehensive evidence of the inhibitory effect of miR-939 on GC metastasis, and suggest a critical role of miR-939 in enhancing GC cell’s sensitivities to 5-Fu based chemotherapy. [score:3]
We observed that miR-939 showed a negative correlation with chemotherapy response in our enrolled cases, in which low expression of miR-939 was observed more frequently in NC + PD subset (41/56, 73.2%) than in CR + PR set (15/56, 26.8%) (P < 0.001, Table  1). [score:3]
b quantification of the colony formation efficiency in miR-939 -overexpressing, miR-939-silenced, and control GC cells treated with 5-Fu chemotherapy. [score:3]
miR-939 inhibits the GC growth in vitro and in vivo. [score:3]
a predicted miR-939 target sequence in 3'UTR of SLC34A2 (SLC34A2-3′UTR) and mutant containing three altered nucleotides in the seed sequence of miR-939 (miR-939-mut). [score:3]
An optimal cutoff value for “high” or “low” miR-939 expression was identified based on the median value of the cohorts of patients tested. [score:3]
Restoration of SLC34A2 abrogated the decreased expression of p-ERK induced by miR-939 in GC cells (lane 3). [score:3]
miR-939 attenuates ERK1/2 phosphorylation and inhibits the Raf-MEK-ERK pathway. [score:3]
To our knowledge, the relationship between miR-939 expression and clinical implication in human cancers has not been analyzed previously. [score:3]
Our data indicate that miR-939 acts as a tumor suppressor miRNA in GC, and miR-939/SLC34A2 axis represents a novel therapeutic strategy for future GC treatment. [score:3]
We detected that reduced expression of miR-939 was associated with chemoresistance and increased risk of tumor recurrence in GC patients. [score:3]
These seemingly contradictory findings suggested a dual role of miR-939 as both a tumor-promoting and -suppressive miRNA, underscoring the need to define the specific role of a miRNA in a certain type of cancer. [score:3]
Expression levels of miR-939 were determined by qRT-PCR and normalized against an endogenous control (U6 RNA). [score:3]
Moreover, a significant increase in level of cleaved caspase-3 and PARP I in miR-939 -overexpressing cells treated with 5-Fu was detected by western blot analysis (Fig.   2d). [score:3]
Interestingly, we found that decreased miR-939 expression is closely related with poor clinical outcome of GC patients. [score:3]
e the same amount (3x10 [6]) of miR-939 -overexpressing and control GC cells were injected subcutaneously into the flanks of nude mice. [score:3]
c comparing differences in the expression levels of miR-939 between GC tumor tissues from recurrent and non-recurrent patients. [score:3]
In this study, we identified SLC34A2 as miR-939 target genes. [score:3]
Mechanistically, we elucidated that miR-939 exerted its function mainly through inhibiting SLC34A2/Raf/MEK/ERK pathway, which is activated in GC. [score:3]
a the wound healing rate in miR-939 -transfected cells was significantly inhibited, while accelerated in miR-939-silenced cells. [score:3]
Our data showed that miR-939 inhibits GC metastasis and enhances the sensitivity of GC cells to 5-fluorouracil (5-Fu) treatment. [score:3]
By conducting the current study, we provide compelling biologic as well as clinical evidence that miR-939 plays a tumor suppressive role in human GC. [score:3]
This also underscored the need to define the differential biologic effects and targets of miR-939 in GC and other cancer types. [score:3]
Moreover, our clinical data show that the expression levels of miR-939 and SLC34A2 were negatively correlated in 112 GC samples (r = −0.623, P < 0.001, Fig.   4e, f). [score:3]
We further identified solute carrier family 34 member 2 (SLC34A2) was a novel target of miR-939. [score:3]
ROC curve analysis for miR-939 expression was performed to assess GC treatment response (area under the curve [AUC] = 0.777, P < 0.001). [score:3]
miR-939 inhibits GC cell metastasis in vitro and in vivo. [score:3]
d miR-939 inhibits tumor metastasis in vivo. [score:3]
To further determine the clinical implication of miR-939 expression, we conducted qRT-PCR assay in 110 pretreatment samples from stage IV GC patients who received palliative chemotherapy. [score:2]
The AnnexinV-PI assay showed that miR-939 -overexpressing cells displayed increased cellular apoptosis and necrosis in response to 5-Fu treatment at 48 h (Fig.   2c). [score:2]
b and c MTT analysis (b) and colony formation assay (c) indicated that restoration of SLC34A2 in miR-939 -overexpressing GC cells recovered cellular proliferation and tumorigenicity ability. [score:2]
Our findings strongly suggest that miR-939 could be used for the development of novel combinatorial therapy strategies aimed at overcoming chemo-resistance and compromising metastasis in GC. [score:2]
To explore miR-939 expression in GC, we conducted real-time PCR assay. [score:2]
e the migratory capacity of miR-939 -overexpressing GC cells was enhanced after transfected with full-length SLC34A2, as assessed by a wound-healing assay. [score:2]
b the number of migrated cell was decreased in miR-939 -overexpressing, while increased in miR-939-silenced GC cells, as assessed by transwell migration assay. [score:2]
miR-939 -overexpressing and vector control cells treated with indicated dose of 5-Fu for 24 h. Cell apoptotic death events were monitored by Annexin V/PI staining and flow cytometry assays. [score:2]
f overexpression of SLC34A2 in miR-939 -transfected cells increased the number of invaded cell, as assessed by a Matrigel invasion assay. [score:2]
MTT and colony formation assays revealed that overexpression of miR-939 significantly increased the growth rate of both GC cell lines; conversely, depletion of miR-939 promoted GC cell proliferation and tumorigenicity in vitro (Fig.   1e, f). [score:2]
c the number of invaded cell was decreased in miR-939 -overexpressing, while increased in miR-939-silenced GC cells, as assessed by Matrigel invasion assay. [score:2]
As shown in Fig.   1a, b, the expression of miR-939 was significantly decreased in human GC cell lines and human primary GC tissues compared with normal gastric epithelial cell lines and nontumor human gastric tissues, respectively (P < 0.05). [score:2]
Number and size of the metastatic colonization were dramatically decreased on the lung surface of miR-939 -transfected cells implanted mice compared to the control mice, and the miR-939 overexpression group exhibited much lower Ki-67 IHC staining of tumor metastases than the control group (Fig.   3d). [score:2]
b luciferase assay of pGL3-SLC34A2-3′-UTR reporters cotransfected with increasing amounts (10, 20, and 50 nM) of miR-939 mimic and mutant oligonucleotides in GC cell lines, or with increasing amounts (20, 50, and 100 nM) of miR-939 inhibitor oligonucleotides in GC cell line. [score:2]
d Annexin V/PI staining assays showed that restoration of SLC34A2 in miR-939 -overexpressing GC cells decreased 5-Fu -induced apoptosis. [score:2]
Importantly, we reported, for the first time, that levels of miR-939 were inversely correlated with local relapse, distant metastasis and chemoresistance in GC patients. [score:1]
As shown in Fig.   2a, b, the combination of 5-Fu with miR-939 was more efficient in reducing the GC cell viability and the clone formation ability. [score:1]
Thus, results suggested that miR-939 could enhance the sensitivity of GC cells to chemotherapies in vivo. [score:1]
More importantly, the combination of miR-939 and 5-Fu is well tolerated by the test animals in vivo, as indicated by mouse body weight (Fig.   2h). [score:1]
We detected that miR-939 levels were significantly decreased in patients who showed local relapse or distant metastasis in comparison to patients who did not have tumor relapse or metastasis during our follow-up period (P < 0.05,Fig. [score:1]
c miR-939 sensitizes GC cells to 5-Fu -induced apoptosis. [score:1]
We evaluated the prognostic significance of miR-939 and SLC34A2 protein expression levels in the GC patients who underwent surgery followed by chemotherapy. [score:1]
However, the clinical significance and biological role of miR-939 in GC is still not known. [score:1]
The observation that miR-939 compromised ERK1/2 activation leads us to further investigate the effect of miR-939 overexpression on RAS-RAF-MEK-ERK pathway. [score:1]
Fig. 6The prognostic significance of miR-939 and SLC34A2 for 112 GC patients assessed by Kaplan-Meier analyses. [score:1]
GC patients with high levels of miR-939 showed better overall survival (OS) rates and lower tumor recurrence rates than those with low miR-939 (Fig.   6a, b); whereas GC patients with high levels of SLC34A2 showed poorer OS rates and higher tumor recurrence rates than those with low SLC34A2 (Fig.   6c, d). [score:1]
Moreover, miR-939 repressed the migration and invasion of GC cells in vitro, and diminished the occurrence of lung metastasis in vivo. [score:1]
The combination of miR-939 and SLC34A2 was an independent prognostic indicator for OS and TTR (P < 0.001, Table  2). [score:1]
Fig. 5Alteration of SLC34A2 levels influences the in vitro effects of miR-939 in GC cells. [score:1]
Therefore, we devised our present study to find out the mechanism of miR-939 action and its potential clinical application in GC. [score:1]
The firefly luciferase construct was cotransfected with a control Renilla luciferase vector into GC cells in the presence of miR-939 mimic, antagomir-939, or miR-control. [score:1]
As expected, restoration of SLC34A2 can block the miR-939-enhanced chemosensitivity and induction of apoptosis by 5-Fu treatment (Fig.   5b-d). [score:1]
In general, these data suggested that miR-939 has a pivotal function in GC pathogenesis, with possible use as a biomarker and intervention point for new therapeutic strategies. [score:1]
miR-939 mimic and antagomir-939 were purchased from GeneCopoeia Company (GuangZhou, China). [score:1]
We further examined whether miR-939 increased the sensitivity of GC cells to 5-Fu by enhancing the rate of apoptosis. [score:1]
TaqMan probes were used to detect miR-939, SLC34A2, U6, and GAPDH (GeneCopoeia, Guangzhou, China). [score:1]
Besides, we provide comprehensive evidence at cellular levels and in the animal mo dels that miR-939 may be beneficial for GC patients with high risks of tumor recurrence and metastasis. [score:1]
GC patients with high miR-939 and low SLC34A2 had the best OS, lowest TTR, and best prognosis. [score:1]
e and fs (e) and colony formation assay (f) indicate that the proliferation and tumorigenicity of miR-939 -overexpressing cells was decreased, and that of the miR-939-silenced cells was increased, compared with control cells. [score:1]
Taken together, these data suggest that SLC34A2 played an important role for the effects of miR-939 on GC cells. [score:1]
This combination gave even better prognostic power than miR-939 or SLC34A2 alone. [score:1]
e and f patients in subgroup I had the (e) longest OS and (f) lowest possibility of tumor recurrence among the four subgroups, which were divided according to combinations of miR-939 and SLC34A2, i. e., I, high miR-939/low SLC34A2; II, high miR-939/high SLC34A2; III, low miR-939/low SLC34A2; IV, low miR-939/high SLC34A2. [score:1]
Next, we sought to determine whether miR-939 sensitized GC cells to 5-Fu treatment, the common used chemotherapeutic drug in GC patients. [score:1]
In contrast, those with low miR-939 and high SLC34A2 had the poorest prognosis with the lowest OS and highest probability of tumor recurrence (P < 0.001; Fig.   6e, f). [score:1]
a and b patients with higher miR-939 had (a) better overall survival (OS) and (b) lower possibility for tumor recurrence. [score:1]
Here, we reported that miR-939 could repress tumor metastasis and increase the sensitivity of tumor cells to chemotherapies in GC. [score:1]
Clinical significance and prognostic values of miR-939 and SLC34A2 in GC patients. [score:1]
Multivariate analysis identified miR-939, SLC34A2, and their combination as independent indicators for poor prognosis and tumor recurrence in GC patients. [score:1]
According to univariate analysis, miR-939, SLC34A2 level, and TNM stage were significantly associated with OS and time to recurrence (TTR) in patients with GC (Table  2), while multivariate analysis confirmed miR-939, SLC34A2 level, and TNM stage as independent prognostic indicators for both OS and TTR (Table  2). [score:1]
miR-939 SLC34A2 Gastric cancer Chemoresistance Metastasis Gastric cancer (GC) is one of the most common causes of cancer-related deaths worldwide [1]. [score:1]
d western blot analysis demonstrated that miR-939 tranfection decreased SLC34A2 protein level of GC cells, while anti-miR-939 dramatically increased SLC34A2 protein in GC cell. [score:1]
Together, these results demonstrate that miR-939 promoted the apoptosis of GC cells. [score:1]
Recently, microarray profiling analysis revealed that a number of miRNAs were dysregulated in human GC samples compared with normal tissues, including miR-939 [13]. [score:1]
In the present study, we observed that miR-939 overerxpression in GC cells significantly decreased MEK1/2 phosphorylation and Raf-1 level, while restoration of SLC34A2 rescued these effects. [score:1]
Our results indicated, for the first time, that the combination of miR-939 and 5-Fu was more efficient in killing GC cells in vitro and in vivo than using miR-939 or 5-Fu alone. [score:1]
[1 to 20 of 120 sentences]
2
[+] score: 38
Figure 1 HuNOS2 [tg] /mNos2 [-/-] mice express both the 3′UTR binding site and a miRNA-939 homolog involved in regulation of the huNOS2 gene. [score:4]
While C57Bl/6 mice express miRNA-939, they lack the binding site in the gene and the additional regulatory complexity found in the human NOS2 gene promoter. [score:4]
The discovery of miRNA-939 mediated regulation of human iNOS protein translation by Guo et al. [29] has provided a realistic mechanism to explain a long term conundrum: Why is iNOS mediated production of NO different between human and rodent? [score:4]
To determine if the human NOS2 gene in HuNOS2 [tg] /mNos2 [-/-] mice expressed the appropriate 3′UTR binding sites we PCR amplified the miRNA-939 binding region from DNA isolated from HuNOS2 [tg] /mNos2 [-/-] brain tissue. [score:3]
Guo et al. [31] have shown that miRNA-939 binds to sites in the 3′UTR region of the human NOS2 gene, thereby altering the translation of iNOS protein and reducing NO production. [score:3]
When these sites are bound to miRNA-939, a post-transcriptional repression of iNOS protein expression is initiated and NO production was thereby reduced. [score:3]
Guo, Geller and colleagues found binding sites for a microRNA (miRNA-939) in the 3′untranslated region (UTR) of the human NOS2 gene. [score:3]
HuNOS2 [tg] /mNos2 [-/-]mice show 3′UTR binding sites, miRNA-939 homolog and reduced NO production in vivoGuo et al. [31] have shown that miRNA-939 binds to sites in the 3′UTR region of the human NOS2 gene, thereby altering the translation of iNOS protein and reducing NO production. [score:3]
Our data from HuNOS2 [tg] /mNos2 [-/-] mice clearly show the presence of the binding site for miRNA-939 in the 3′UTR region of the HuNOS2 gene and the presence of a miRNA-939 homolog in the brain, thus recreating a more human-like condition. [score:1]
Figure 1B presents results from a typical PCR cycling reaction and demonstrates the presence of miRNA-939 in HuNOS2 [tg] /mNos2 [-/-] brain. [score:1]
HuNOS2 [tg] /mNos2 [-/-]mice show 3′UTR binding sites, miRNA-939 homolog and reduced NO production in vivo. [score:1]
Figure 1C shows the average fold change (±sem) in miRNA-939 in brain and liver samples after stimulation with LPS. [score:1]
A similar LPS -mediated increase in miRNA939 levels was shown by Guo et al. [29] for human hepatocytes in culture and in liver lysates from WT mice injected with LPS or a cytokine mix. [score:1]
We also examined the effect of on the level of miRNA-939 homolog in our mice. [score:1]
The lower band corresponds to a 185 bp product containing the 3′UTR miRNA-939 binding region of huNOS2 gene. [score:1]
Having demonstrated that HuNOS2 [tg] /mNos2 [-/-] mice express the 3′UTR binding site that is characteristic of the human NOS2 gene, we then used RT-PCR to detect the presence of a miRNA-939 homolog in brain and liver lysates from lipopolysaccharide (LPS)- treated HuNOS2 [tg] /mNos2 [-/-] mice. [score:1]
A- PCR amplification of the 3′UTR region containing putative binding sites for miRNA-939 of the human NOS2 gene in HuNOS2 [tg] /mNos2 [-/-] and WT mice. [score:1]
We also identified miRNA-939, the binding partner for this site, in mouse brain lysates and further demonstrated reduced levels of nitric oxide (NO) typical of the human immune response on injection with lipopolysaccharide (LPS). [score:1]
B- Graph of PCR product amount versus cycle number for amplification of miRNA-939 homolog product using small nucleolar (sno) RNA-202 as endogenous controls. [score:1]
[1 to 20 of 19 sentences]
3
[+] score: 10
For example, a bioinformatics -based prediction indicates that hsa-miR-939 can target vascular endothelial growth factor A (VEGF A), inducible nitric oxide synthase 2A, and the alpha subunit of voltage-gated sodium channel type IV and that hsa-miR-25 can target endothelin receptor type B. Since one of the predicted gene targets for hsa-miR-939 is VEGF A, the upregulation of VEGF in the serum of CRPS patients strengthens the prediction. [score:10]
[1 to 20 of 1 sentences]
4
[+] score: 10
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
control Expression in case group 1 hsa-mir-1290 0.26 down 2 hsa-mir-342-5p 0.22 down 3 hsa-mir-1224-5p 0.23 down 4 hsa-mir-345 0.38 down 5 hsa-mir-1228 0.38 down 6 hsa-mir-1249 0.32 down 7 hsa-mir-1826 0.26 down 8 hsa-miR-1306 0.38 down 9 hsa-miR-188-5p 0.43 down 10 hsa-miR-320a 0.48 down 11 hsa-miR-320c 0.26 down 12 hsa-miR-365 0.31 down 13 hsa-miR-423-5p 0.35 down 14 hsa-miR-483-5p 0.25 down 15 hsa-miR-634 0.31 down 16 hsa-miR-671-5p 0.23 down 17 hsa-miR-939 0.24 down 18 hsa-miR-1246 2.22 up 19 hsa-miR-150 10.41 up 20 hsa-miR-574-5p 8.04 up Table 3 MiRNAs Target Gene Symbol hsa-miR-345PUM2, PPP2R3A, BCAT1, ZFHX4, CHSY3, ARNT, SHE, SLC7A5, SOS1,. [score:5]
[1 to 20 of 2 sentences]
5
[+] score: 9
A validation study was done to corroborate a subset of the results, including expression levels of miR-4299, miR-196b, miR-324-5p, miR-455-3p and miR-939, through analyzing stage IV colon adenocarcinoma tissues (not responding and responding to the chemotherapy) with laser capture microdissection and quantitative real-time PCR. [score:3]
Secondly, in most of miRNAs we identified (miR-196b, miR-4299, miR-324-5p, miR-455-3p and miR-939), the potential linkage between their expression and chemoresistance was already established; then some of them were identified for the first time. [score:3]
Fig.  2 Dots indicate of the relative quantification (RQ) values of miRNA expression levels (a miR-4299, b miR-196b, c miR-324-5p, d miR-455-3p, e miR-939), normalized by U6. [score:3]
[1 to 20 of 3 sentences]
6
[+] score: 7
Start position 530 was targeted by hsa-miR-3131, hsa-miR-4298, and hsa-miR-939 while position 531 was targeted by hsa-miR-134 and hsa-miR-3180-3p. [score:5]
The start binding positions 304 of hsa-miR-762 and 308 of hsa-miR-3677 were highly conserved among more than five hundred NS1 genes in type 2 while positions 765 of hsa-miR-637 and 773 of hsa-miR-3663-5p were highly conserved among almost three hundred NS1 sequences in dengue type 3. More than two hundred nucleoprotein (NP) genes of rabies virus were predicted with highly conserved start binding positions 122 of hsa-miR-939, 359 of hsa-miR-770-5p, and 820 of hsa-miR-2277-3p and hsa-miR-638. [score:1]
The start binding positions 304 of hsa-miR-762 and 308 of hsa-miR-3677 were highly conserved among more than five hundred NS1 genes in type 2 while positions 765 of hsa-miR-637 and 773 of hsa-miR-3663-5p were highly conserved among almost three hundred NS1 sequences in dengue type 3. More than two hundred nucleoprotein (NP) genes of rabies virus were predicted with highly conserved start binding positions 122 of hsa-miR-939, 359 of hsa-miR-770-5p, and 820 of hsa-miR-2277-3p and hsa-miR-638. [score:1]
[1 to 20 of 3 sentences]
7
[+] score: 6
The incubation of NHDF cell cultures for 2 hours with a biological drug leads to changes in the expression of 12 miRNAs (hsa-miR-1231, hsa-miR-1275, hsa-miR-143, hsa-miR-16, hsa-miR-1909, hsa-miR-196a, hsa-miR-199a-5p, hsa-miR-22, hsa-miR-3162, hsa-miR-34a, hsa-miR-382, and hsa-miR-939), regulating the expression of the analysed transcripts. [score:6]
[1 to 20 of 1 sentences]
8
[+] score: 4
For H1N1 infected cells, at 18 and 24-hour post-infection, miR-188-5p, miR-1260, miR-1274a, miR-1274b, miR141, miR183*, miR-18b, miR-19a, miR21*, miR-301a, miR-572, miR-720, and miR-939 were found to be up-regulated (>1.5-fold, p<0.05) (Table 1). [score:4]
[1 to 20 of 1 sentences]
9
[+] score: 3
A recent screen for miRNAs, which target the 3′ UTR of TNF mRNA, revealed miR-125b and miR-939 as further candidates. [score:3]
[1 to 20 of 1 sentences]
10
[+] score: 3
Additionally, the expression level of miR-939 in HCC derived from CH was significantly lower than in HCC from LC (Table  3). [score:3]
[1 to 20 of 1 sentences]
11
[+] score: 2
Ying X. Li-ya Q. Feng Z. Yin W. Ji-hong L. MiR-939 promotes the proliferation of human ovarian cancer cells by repressing APC2 expressionBiomed. [score:2]
[1 to 20 of 1 sentences]
12
[+] score: 2
Additionally, miR-26a and miR-939 regulate the replication of H1N1 influenza virus in MDCK cells [48]. [score:2]
[1 to 20 of 1 sentences]
13
[+] score: 1
Other miRNAs from this paper: hsa-mir-15a, hsa-mir-1234
Additionally, genes (in multiple matchings) PVT1 and UBD and CPSF1, MIR1234, MIR939, DLEU2, MIR15A, FCGR1A, FCGR1B, GABBR1, ZNF131, MATR3 and SNHG4 are identified to be related and possibly related to cancer, respectively. [score:1]
[1 to 20 of 1 sentences]
14
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-100, hsa-mir-101-1, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-215, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-194-1, hsa-mir-195, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-130b, hsa-mir-302c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-324, hsa-mir-451a, hsa-mir-483, hsa-mir-484, hsa-mir-486-1, hsa-mir-500a, hsa-mir-92b, hsa-mir-595, hsa-mir-596, hsa-mir-421, hsa-mir-378d-2, hsa-mir-744, hsa-mir-885, hsa-mir-940, hsa-mir-1229, hsa-mir-1233-1, hsa-mir-1290, hsa-mir-1246, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-4286, hsa-mir-500b, hsa-mir-1233-2, hsa-mir-3935, hsa-mir-642b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j, hsa-mir-486-2
Similarly, other groups have identified several circulating miRNAs as non-invasive diagnostic biomarkers, such as miR-21, miR-122, miR-223, miR-15b, miR-130b, miR-101, miR-483, miR-125, miR-143, miR-215, miR-200, miR-939, and miR-595 [44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56]. [score:1]
[1 to 20 of 1 sentences]
15
[+] score: 1
Besides, miR-16 and miR-939 were confirmed to be contributed to the chemotherapy response of GC [17, 18]. [score:1]
[1 to 20 of 1 sentences]