Abstract:Osteosarcoma (OS) is the most common form of bone malignancy in children and adolescents. A class of molecules known as microRNAs (miRNAs) have been routinely associated in the development and progression of OS. The present study was centered on the less well-known miRNA, miRNA (miR)-150, and its role in OS was investigated. The levels of miR-150 were examined in 40 tissue specimens from patients with OS and adjacent normal tissues using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) an… Show more
“…More convincingly, the facilitative effect of NEAT1 on ROCK1 could be attenuated by an elevation of miR‐382‐3p (co‐transfection of wt‐pcDNA‐NEAT1 and miR‐382‐3p mimics) (Figure B). As reported previously, ROCK1 was also targeted by other miRNA like miR‐340, miR‐150 . Here, we measured the expression of miR‐340 and miR‐150 as well by qRT‐PCR.…”
Long non‐coding RNA (lncRNA) are extensively involved in various malignant tumors, including ovarian cancer (OC). In the present study, we focused on the expression and function of nuclear enriched abundant transcript 1 (NEAT1) in OC cells’ metastasis. We demonstrated that NEAT1 was upregulated in OC tissue specimens and cell lines. In addition, we revealed that depression of NEAT1 inhibited OC cells’ metastasis and the expression of Rho associated coiled‐coil containing protein kinase 1 (ROCK1), which is a metastasis‐related gene. Using online predictive software and a series of luciferase assays, we demonstrated that both NEAT1 and ROCK1 were the targets of microRNA‐382‐3p (miR‐382‐3p) and share similar microRNA responding elements (MRE). Furthermore, we illustrated that NEAT1 and miR‐382‐3p inhibited each other in a reciprocal manner. Finally, through antisense experiments we demonstrated that NEAT1 promoted ROCK1‐mediated metastasis by functioning as a ceRNA of miR‐382‐3p. In summary, the findings of this study revealed that NEAT1 promoted OC cells’ metastasis through regulating the miR‐382‐3p/ROCK1 axial. The present study might provide a new target for treating OC.
“…More convincingly, the facilitative effect of NEAT1 on ROCK1 could be attenuated by an elevation of miR‐382‐3p (co‐transfection of wt‐pcDNA‐NEAT1 and miR‐382‐3p mimics) (Figure B). As reported previously, ROCK1 was also targeted by other miRNA like miR‐340, miR‐150 . Here, we measured the expression of miR‐340 and miR‐150 as well by qRT‐PCR.…”
Long non‐coding RNA (lncRNA) are extensively involved in various malignant tumors, including ovarian cancer (OC). In the present study, we focused on the expression and function of nuclear enriched abundant transcript 1 (NEAT1) in OC cells’ metastasis. We demonstrated that NEAT1 was upregulated in OC tissue specimens and cell lines. In addition, we revealed that depression of NEAT1 inhibited OC cells’ metastasis and the expression of Rho associated coiled‐coil containing protein kinase 1 (ROCK1), which is a metastasis‐related gene. Using online predictive software and a series of luciferase assays, we demonstrated that both NEAT1 and ROCK1 were the targets of microRNA‐382‐3p (miR‐382‐3p) and share similar microRNA responding elements (MRE). Furthermore, we illustrated that NEAT1 and miR‐382‐3p inhibited each other in a reciprocal manner. Finally, through antisense experiments we demonstrated that NEAT1 promoted ROCK1‐mediated metastasis by functioning as a ceRNA of miR‐382‐3p. In summary, the findings of this study revealed that NEAT1 promoted OC cells’ metastasis through regulating the miR‐382‐3p/ROCK1 axial. The present study might provide a new target for treating OC.
“…MiRNAs are key regulators in the tumorigenesis of OS. Some miRNAs are down-regulated in OS, such as miR-133a, 24 -137, 25 -150, 26 -223, 27 -505, 28 and -564. 29 In consistent with these miRNAs, miR-431-5p was also down-regulated in OS tissues and cells in this study.…”
Purpose
This study aimed to evaluate the regulatory role of miR-431-5p on the tumorigenesis of osteosarcoma (OS) and the underlying mechanism involving
pannexin 3
(
PANX3
).
Methods
qRT-PCR was applied to measure the expression of miR-431-5p in OS tissues and cells.
PANX3
and miR-431-5p were overexpressed in U2OS and HOS cells. The cell viability and apoptosis were determined by MTT and FITC/PI double staining assay, respectively. Transwell assay was performed to detect cell migration and invasion. The protein expression of cleave-caspase-3 and MMP-2/-9 was detected by Western blot. The target relationship between miR-431-5p and
PANX3
was predicated by ENCORI and identified by DLR assay. The anti-tumor effect of miR-431-5p was further analyzed in a xenograft tumor model in mice.
Results
MiR-431-5p expression was down-regulated in OS tissues and negatively correlated with lymph node metastasis and TNM stage. Over-expression of miR-431-5p induced cell apoptosis, inhibited cell proliferation, migration and invasion, up-regulated cleave-caspase-3, and down-regulated MMP-2 and -9 in OS cells. Over-expression of miR-431-5p also inhibited the growth of tumor xenografts in mice. In addition,
PANX3
was a target of miR-431-5p. Over-expression of
PANX3
reversed the anti-tumor effect of miR-431-5p mimics on U2OS and HOS cells.
Conclusion
Up-regulation of miR-431-5p suppressed the tumorigenesis of OS via targeting
PANX3
.
“…morphogenesis, 9 Parkinson's disease, 10 and differentiation. 11 Recently, increasing evidence has indicated a critical role for miRNAs on neuropathic pain.…”
mentioning
confidence: 99%
“…MiR-150 has been reported to be involved in various processes of disease. 9,16 For example, miR-150 can restrain dendritic cell immune inflammatory responses and cardiomyocyte apoptosis via targeting JAK1-STAT1/ c-Fos pathway. 16 MiR-150 is decreased in osteosarcoma and suppresses cell proliferation, migration, and invasion by targeting ROCK1.…”
MicroRNAs (miRNAs) are reported as vital participators in the pathophysiological course of neuropathic pain. However, the underlying mechanisms of the functional roles of miRNAs in neuropathic pain are largely unknown. This study was designed to explore the potential role of miR-150 in regulating the process of neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI). Overexpression of miR-150 greatly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including COX-2, interleukin IL-6, and tumor necrosis factor (TNF)-α in CCI rats. By bioinformatic analysis, 3′-untranslated region (UTR) of Tolllike receptor (TLR5) was predicted to be a target of miR-150. TLR5 commonly serves as an important regulator of inflammation. Overexpression of miR-150 significantly suppressed the expression of TLR5 in vitro and in vivo. Furthermore, upregulation of TLR5 decreased the miR-150 expression and downregulation of TLR5 increased miR-150, respectively. Overexpression of TLR5 significantly reversed the miR-150-induced suppressive effects on neuropathic pain. In conclusion, our current study indicates that miR-150 may inhibit neuropathic pain development of CCI rats through inhibiting TLR5-mediated neuroinflammation. Our findings suggest that miR-150 may provide a novel therapeutic target for neuropathic pain treatment.
K E Y W O R D Schronic constriction injury, miR-150, neuropathic pain, TLR5
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