19 publications mentioning hsa-mir-873

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-873. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1

Set 2 is the list of predicted targets of miRs tested to not inhibit NALM6 growth (i. e. miR-550a, miR-873, miR-381 and miR-432) from TargetScan6.2 or miRDB, while Set 3 is the list of mRNA that is expressed in NALM6, as determined by genome-wide microarray profiling downloaded from the Cancer Cell Line Encyclopedia and its expression levels are denoted in the microarray dataset as “marginal” or “present”.

First, we downloaded the sets of predicted mRNA targets of miR-509-5p and miR-509-3p (Set 1), as well as those of the 4 miRs that we had shown not to inhibit NALM6 growth (i. e. miR-381, miR-432, miR-550a and miR-873; Set 2) from the TargetScan6.2 [37] and/or miRDB [38], [39] miR target prediction databases.

These results indicate that miR-381, miR-432, miR-550a, and miR-873 do not inhibit growth of NALM6.

4 miRs (miR-381, miR-509, miR-550a, and miR-873) and 1 miR cluster (miR-432∼136) inhibited NALM6 growth in at least 2 of 3 replicate screens performed.

Similarly, overexpression of miR-381, miR-550a, miR-873, and miR-432 was achieved by lentiviral transduction (Figure S1E).

NALM6 cells were individually transduced with lentivirus of (A) miR-381; (B) miR-550a; (C) miR-873 and (D) miR-432∼136 and empty vector (EV#1) to MOI  = 2. At 7 days after transduction, cells were mixed with mock-transduced cells to 50% GFP [+] cells and this was set as Day 0. The %GFP [+] cells (pre-gated on viable cells) of each culture were assessed weekly by flow cytometry for 35 days.

Similarly, no change in %GFP [+] cells was observed over 35 days in thes for miR-381, miR-550a, miR-873 and miR-432∼136 (Figure S1A-S1D).

2

In our microarray study, seven miRNAs were found to be differentially expressed, four (hsa-miR-196b, hsa-miR-30a, hsa-miR-873, and hsa-miR-337-3p) were downregulated and three (hsa-miR-1288, hsa-miR-451, and hsa-miR-223) were upregulated in EP pregnancy-derived tissues compared to VTOP samples.

Four miRNAs (hsa-miR-196b, hsa-miR-30a, hsa-miR-873, and hsa-miR-337-3p) were found to be downregulated in EP versus healthy pregnancy tissues, and three miRNAs (hsa-miR-1288, hsa-miR-451, and hsa-miR-223) were upregulated in EP compared to control pregnancy tissue samples (Figure 1A).

3

It is conceivable that several of the down-regulated miRNAs with no defined functions at this point (i. e., miR-873, miR-95, miR-543) may exhibit tumor suppressor activity and normally target components of key signaling pathways that promote and maintain the growth and survival of glioma cells as has recently been reported for miR-10b [17].

We identified several new miRNAs that were not previously reported to be dysregulated in glioblastomas, including miR-95, miR-543, miR-598, and miR-873 (Fig. 1, Table S6).

miR-598, and miR-873) that were not previously reported to be dysregulated in brain cancers (Table S6).

4

MiR-485 has been implicated in synaptic formation and maintenance and has been reported to be dysregulated in Alzheimer’s disease and Huntington’s disease [32], miR-124 is known as a neurodevelopmental regulator [33], miR-219 required for neural precursor differentiation in zebrafish [34] and promotes myelination in rats [35], miR-127 regulates cell proliferation and senescence by targeting BCL6 [36] while miR-136, miR-873 and miR-410 have all been studied in the context of glioma growth, invasiveness and apoptosis 37– 39.

miRNAlog [2]FoldChange P-value Corrected P-value hsa-mir-577 −3,28 1,46E-10 3,87E-08 hsa-mir-182-5p −2,70 6,50E-15 3,44E-12 hsa-mir-485-5p −2,12 8,79E-05 8,45E-03 hsa-mir-124-3p −1,83 1,05E-05 1,85E-03 hsa-mir-218-5p −1,68 1,54E-04 1,16E-02 hsa-mir-183-5p −1,62 3,14E-04 2,08E-02 hsa-mir-873-5p −1,58 9,80E-04 3,25E-02 hsa-mir-133a −1,53 6,05E-04 2,29E-02 hsa-mir-487b −1,45 1,56E-03 4,59E-02 hsa-mir-219-5p −1,44 9,55E-04 3,25E-02 hsa-mir-409-3p −1,34 1,12E-03 3,48E-02 hsa-mir-889 −1,23 5,71E-04 2,29E-02 hsa-mir-136-3p −1,15 1,75E-03 4,87E-02 hsa-mir-410 −1,12 4,02E-04 2,29E-02 hsa-mir-127-3p −0,95 5,61E-04 2,29E-02 hsa-mir-148a-3p 1,23 4,99E-04 2,29E-02 hsa-mir-155-5p 1,82 9,56E-05 8,45E-03 hsa-mir-221-3p 2,10 4,82E-04 2,29E-02For each differently expressed miRNA we report the standard name according to MirBase database, the log [2] fold-change, the P-value and the corresponding corrected P-value as calculated by DESeq.

5

Six miRNAs, 3 less expressed (miR-324-3p, miR-516a-3p, miR-659-3p) and 3 more expressed (miR-137, miR-301a-3p, miR-873-5p) in BM-infiltrating cells than in primary tumors, were significantly differentially expressed also in this new set of samples (Table 2).

To validate the differential expression of the selected 20 miRNAs, reverse-transcribed and pre-amplified miRNA fractions from 10 additional BM-infiltrating and 10 primary tumors were amplified in a 96 well plate in triplicate using the specific TaqMan [©] human microRNA assays (hsa-miR-324-3p, catalog #002161; hsa-miR-516-3p, catalog #001149; hsa-miR-628-5p, catalog #002433; hsa-miR-659-3p, catalog #001514; hsa-miR-10b, catalog #002218; hsa-miR-128, catalog #002216; mmu-miR-137, catalog #01129; mmu-miR-140, catalog #001187; hsa-miR-16, catalog #000391, hsa-miR-191, catalog #002299; hsa-miR-301, catalog #000528; hsa-miR-361-3p, catalog #002116; hsa-miR-365, catalog #001020; hsa-miR-548d-3p, catalog #001605; hsa-miR-572, catalog #001614; hsa-miR-576-5p, catalog #002350, hsa-miR-616, catalog #001589; hsa-miR-628-3p, catalog #002434; hsa-miR-873, catalog #002356; hsa-miR-98, catalog #000577; U6 snRNA, catalog #001973, Life Technologies).

6

Four miRNAs were differentially down-regulated (hsa-mir-196b, hsa-mir-30a, hsa-mir-873, and hsa-mir-337-3p) while three were upregulated (hsa-mir-1288, hsa-mir-451, and hsa-mir-223) in women suffering from EP compared to normal pregnancies.

For detecting EP, miR-873 presented the highest sensitivity as a single marker (61,76%) and combined with hCG and progesterone revealed a sensitivity of 79.41% (at a fixed specificity of 90%).

Thus, the authors suggested miR-873 as a single, noninvasive and stable marker for early EP detection [46].

Out of the 21 miRNAs, miR-873 and miR-223 were significantly lower in EP than in SA and VIP, while miR-323 was significantly higher in EP.

7

For example, the lncRNA NRF regulates programmed necrosis and myocardial injury during ischaemia and reperfusion by targeting miR-873; MEG3 promotes hepatic insulin resistance via increasing FoxO1 expression; and Lnc-CC3 increases metastasis in cervical cancer by increasing Slug expression 32 33.

8

Specifically, Tax downregulated miR-149 and miR-873, both of which directly target p300 and P/CAF [48].

9

miR-873 acts as a novel sensitizer of glioma cells to cisplatin by targeting Bcl-2. Int.

For instance, miR-873 was found to enhance the sensitivity of glioma cells to cisplatin by targeting Bcl-2 (Chen et al., 2015).

10

In addition, miR-29c, miR-873 and let-7 have been reported to suppress A20 expression, therefore contributing to the activation of NF-kB signaling [24– 26].

11

[10] Li et al. [11] also found that miRNA-873 inhibited morphine -induced macrophage apoptosis by elevating A20 expression.

12

The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.

13

The microRNA profile in these male brains included significant downregulation of miR-322, miR-574, and miR-873, showing similarity to control female brains [65].

14

Among those upregulated miRNAs by Tax, we focused on miRNAs known to play a key role in oncogenesis and chemoresistance such as miRlet7-a, miR16, miR20, miR 21, miR31, miR93, miR125a, miR132, miR143, miR155,miR200 and miR873 [22, 23].

15

34 hsa-miR-335 −0.35hsa-miR-345 [44], [53], [71] 1.16 hsa-miR-363 0.99 hsa-miR-371-5p 0.55 hsa-miR-421 0.50 hsa-miR-483-5p 1.33 hsa-miR-494 0.87 hsa-miR-505* −0.40 hsa-miR-513a-5p 1.06 hsa-miR-513b 1.19 hsa-miR-513c 1.22 hsa-miR-551b −0.40 hsa-miR-574-5p 0.97hsa-miR-630 [68], [73] 0.96 hsa-miR-769-5p −0.34 hsa-miR-801 0.66 hsa-miR-873 −0.64 hsa-miR-877* 0.72 hsa-miR-923 0.89 hsa-miR-940 0.49 hsa-miR-95 −0.44 hsa-miR-99a −0.64Irradiated and non-irradiated PBL of the same donors were incubated in static gravity (1 g) for 4 and 24 h, and miRNA expression profile was analyzed at the end of each incubation time.

16

01 Stress response, cell proliferation miR-542 ↓2.60 NA miR-574 ↑2.09 Inflammation (Tlr9 activation), cell proliferation, apoptosis miR-669j ↑3.12 NA miR-672 ↑2.40 NA miR-674 ↑2.19 NA miR-744 ↑4.35Oncogene (Tgf) suppression miR-873 ↑2.53 ↑3.22 NA miR-1930 ↑3.31 NA miR-1934 ↑2.17 ↑3.27 NA miR-1942 ↑2.49 NA miR-3064 ↑2.50 NA miR-3065 ↑3.20 NA miR-3069 ↑2.98 NA miR-3071 ↑3.51 NA miR-3073 ↓2.78 NA miR-3092 ↑3.48 NA miR-3093 ↑3.28 NA miR-3109 ↓2.07 NAAll reported variations were statistically significant (P < 0.05).

17

8 of the 40 Drosophila miRNAs with ≥70% homologous sequences in humans show extensive overall similarity with 5′ mismatches: dme-miR-8 with hsa-miR-141 and hsa-miR-200a, dme-miR-10 with hsa-miR-100 and hsa-miR-99a, dme-miR-100 with hsa-miR-10a and hsa-miR-10b, dme-miR-125 with hsa-miR-10a and hsa-miR-10b, dme-miR263a with hsa-miR-183, dme-miR-263b with hsa-miR-183, dme-miR-306 with hsa-miR-873, and dme-miR-993 with hsa-miR-100*.

18

MiR-26a and miR-873 stimulate production of pro-inflammatory cytokines, affecting the neuroinflammatory process and severity of EAE.

19

73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32.