Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA-886 suppresses osteosarcoma cell proliferation and its maturation is suppressed by long non-coding RNA OXCT1-AS1.

ABSTRACT: This study aimed to investigate the roles of microRNA-886 (miR-886) and long non-coding RNA (lncRNA) OXCT1-AS1 in osteosarcoma (OS). We predicted that they might interact with each other. The expression of OXCT1-AS1 and miR-886 (mature and premature) in osteosarcoma and paired non-tumor tissues from 66 OS patients was negatively correlated. Overexpression and silencing assays showed that OXCT1-AS1 suppresses miR-886 maturation. RNA-RNA pulldown and subcellular fractionation assays demonstrated the direct interaction between OXCT1-AS1 and miR-886. BrdU proliferation assays revealed that OXCT1-AS1 promoted OS cell proliferation, and miR-886 reduced the enhancing effects of OXCT1-AS1 on OS cell proliferation. Western blot showed that OXCT1-AS1 had no effects on the levels of epithelial-mesenchymal transition biomarkers. Overall, OXCT1-AS1 suppresses miR-886 maturation to promote OS cell proliferation.

SUBMITTER: Dai W

PROVIDER: S-EPMC8973740 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

MicroRNA-886 suppresses osteosarcoma cell proliferation and its maturation is suppressed by long non-coding RNA OXCT1-AS1.

Dai Wen W Liu Han H

Bioengineered 20220301 3

This study aimed to investigate the roles of microRNA-886 (miR-886) and long non-coding RNA (lncRNA) OXCT1-AS1 in osteosarcoma (OS). We predicted that they might interact with each other. The expression of OXCT1-AS1 and miR-886 (mature and premature) in osteosarcoma and paired non-tumor tissues from 66 OS patients was negatively correlated. Overexpression and silencing assays showed that OXCT1-AS1 suppresses miR-886 maturation. RNA-RNA pulldown and subcellular fractionation assays demonstrated t ...[more]

PMID: 35191809

Similar Datasets

MicroRNA-448 suppresses osteosarcoma cell proliferation and invasion through targeting EPHA7.

Project description:Osteosarcoma is the most common type of malignant bone tumor, often affecting adolescents and children. MicroRNAs (miRNAs) are a group of small, non-protein coding, endogenous RNAs that play critical roles in osteosarcoma tumorigenesis. In our study, we demonstrated that miR-448 expression was downregulated in osteosarcoma tissues and cell lines. Overexpression of miR-448 suppressed osteosarcoma cell proliferation, colony formation and migration. Moreover, we found that EPHA7 was a direct target gene of miR-448 in osteosarcoma cells. We further demonstrated that the EPHA7 expression level was upregulated in osteosarcoma tissues. Interestingly, the expression level of EPHA7 was inversely correlated with the expression level of miR-448 in osteosarcoma tissues. In addition, elevated expression of miR-448 suppressed osteosarcoma cell proliferation and invasion through targeting EPHA7. Taken together, these findings suggest that miR-448 functioned as a tumor suppressor gene in the development of osteosarcoma through targeting EPHA7.

| S-EPMC5467824 | biostudies-literature

MicroRNA-100 suppresses human osteosarcoma cell proliferation and chemo-resistance via ZNRF2.

Project description:Osteosarcoma (OS) is a prevalent cancer worldwide. MicroRNAs (miRNAs) play critical roles in the growth, invasion and carcinogenesis of OS, whereas the underlying mechanisms remain ill-defined. Here, we addressed these questions. We detected significantly higher levels of ZNRF2, a ubiquitin ligase of the RING superfamily, and significantly lower levels of miR-100 in the OS specimens, compared to the paired normal bone tissues. The levels of ZNRF2 and miR-100 inversely correlated in the OS specimens. In addition, low miR-100 levels are associated with poor prognosis of the OS patients. Either ZNRF2 overexpression or miR-100 depletion increased in vitro OS cell growth and improved cell survival at the presence of Doxorubicin. Mechanistically, with the help of bioinformatics analysis and luciferase-reporter assay, we found that miR-100 might bind to the 3'-UTR of ZNRF2 mRNA to prevent its protein translation. Thus, our data suggest that re-expression of miR-100 may inhibit OS cell growth and decrease OS cell chemo-resistance.

| S-EPMC5471002 | biostudies-literature

MicroRNA-503 suppresses cell proliferation and invasion in osteosarcoma via targeting insulin-like growth factor 1 receptor.

Project description:MicroRNAs (miRs) are a class of small non-coding RNAs and have key roles in various cancer types. Recently, miR-503 has been reported to act as a tumor suppressor in osteosarcoma. However, the detailed mechanism of the regulatory role of miR-503 in osteosarcoma cell proliferation and invasion has largely remained elusive. The present study found that miR-503 was significantly downregulated in osteosarcoma tissues compared to that in matched adjacent non-tumorous tissues. In addition, the expression of miR-503 in osteosarcoma of T3-T4 stage was significantly lower when compared with that in T1-T2 stage samples. miR-503 was also downregulated in osteosarcoma cell lines (Saos-2, MG63, U2OS and SW1353), when compared with that in the normal osteoblast cell line hFOB. Overexpression of miR-503 significantly inhibited the proliferation and invasion of U2OS cells and decreased the protein levels of insulin-like growth factor 1 receptor (IGF-1R), which was further identified as a novel target of miR-503 by a luciferase reporter assay. Moreover, overexpression of IGF-1R eliminated the suppressive effects of miR-503 on the proliferation and invasion of U2OS cells, suggesting that miR-503 inhibits osteosarcoma cell proliferation and invasion by directly targeting IGF-1R. Furthermore, IGF-1R was significantly upregulated in osteosarcoma tissues compared with that in adjacent non-tumor tissues, as well as in osteosarcoma cell lines compared with that in hFOB cells. In addition, the expression levels of IGF-1R were inversely correlated to the miR-503 levels in osteosarcoma tissues, suggesting that the increased IGF-1R expression may be caused by the reduced expression of miR-503. In conclusion, the present study demonstrated that miR-503 suppresses cell proliferation and invasion in osteosarcoma via targeting IGF-1R and thus highlights the importance of miR-503/IGF-1R signaling in the malignant progression of osteosarcoma.

| S-EPMC5526065 | biostudies-other

Long non-coding RNA FOXD2-AS1 contributes to colorectal cancer proliferation through its interaction with microRNA-185-5p.

Project description:Emerging evidence has indicated that long non-coding RNA plays an important role in carcinogenesis at the transcriptional and post-translational levels. The regulation of carcinogenesis-related effectors is potent in the determination of tumor initiation and progression. In the current study, FOXD2-AS1 was found to interact with microRNA (miR)-185-5p to modulate proliferation, migration, and invasion of colorectal cancer (CRC) cells. Interestingly, expression of cell division control 42 was significantly influenced by FOXD2-AS1 and miR-185-5p. In CRC patients, the expression level of FOXD2-AS1 in CRC tissue was closely associated with miR-185-5p and cell division control 42, and implicated in the overall survival rate. Therefore, our study suggests that long non-coding RNA FOXD2-AS1 plays a positive role in CRC and could be developed and used as a potential biomarker for the diagnosis and therapy of CRC. This will greatly improve the prevention and treatment of the third most common cancer worldwide.

| S-EPMC6029818 | biostudies-literature

MicroRNA-379 suppresses osteosarcoma progression by targeting PDK1.

Project description:Osteosarcoma is the most common primary bone tumour. Increasing evidence has demonstrated the pathogenic role of microRNA (miRNAs) dysregulation in tumour development. miR-379 was previously reported to function as an oncogenic or tumour-suppressing miRNA in a tissue-dependent manner. However, its function in osteosarcoma remains unknown. In this study, we found that the expression of miR-379 was downregulated in osteosarcoma tissues and cell lines. Further functional characterization revealed that miR-379 suppressed osteosarcoma cell proliferation and invasion in vitro and retarded the growth of osteosarcoma xenografts in vivo. Mechanistically, PDK1 was identified as the direct target of miR-379 in osteosarcoma, in which PDK1 expression was up-regulated and showed inverse correlation with miR-379. Enforced expression of PDK1 promoted osteosarcoma cell proliferation and rescued the anti-proliferative effect of miR-379. These data suggest that miR-379 could function as a tumour-suppressing miRNA via targeting PDK1 in osteosarcoma.

| S-EPMC5264134 | biostudies-literature

Long non-coding RNA HNF1A-AS1 promotes proliferation and suppresses apoptosis of bladder cancer cells through upregulating Bcl-2.

Project description:Emerging evidences have indicated that long non-coding RNAs (lncRNAs) are pivotal regulators of tumor development and progression. HNF1A-AS1 (HNF1A antisense RNA 1, C12 or f27) is a novel long non-coding RNA that acts as a potential biomarker and is involved in development and progression of several cancers. Nevertheless, we know nothing about the clinical significance and molecular mechanism of HNF1A-AS1 in bladder cancer. In this study, we found that HNF1A-AS1 is significantly up-regulated in bladder cancer. Further experiments had demonstrated that silencing HNF1A-AS1 in bladder cancer cells could inhibit the proliferation and induce apoptosis. Mechanistically, we found down-regulated of HNF1A-AS1 increased the expression of miR-30b-5p and subsequently inhibited the expression of Bcl-2, in a ceRNA-dependent way. Moreover, knockdown of miR-30b-5p reversed cell proliferation inhibition and cell apoptosis induced by silencing HNF1A-AS1. In conclusions, we demonstrated that HNF1A-AS1 plays an important regulatory role in bladder cancer and shed new light on lncRNA-directed diagnostic and therapeutics in bladder cancer.

| S-EPMC5652733 | biostudies-literature

CXCR4-mediated osteosarcoma growth and pulmonary metastasis is suppressed by MicroRNA-613.

Project description:Osteosarcoma is the most common primary bone malignancy. Recently, studies showed chemokine receptor 4 (CXCR4) played a critical role in osteosarcoma. However, the regulation of CXCR4 is not fully understood. microRNAs are short, non-coding RNAs that play an important roles in post-transcriptional regulation of gene expression in a variety of diseases including osteosarcoma. miR-613 is a newly discovered miRNA and has been reported to function as a tumor suppressor in many cancers. In this study, we confirmed that both Stromal Cell-Derived Factor (SDF-1) and CXCR4 could be prognostic markers for osteosarcoma. Meanwhile this study found that SDF-1/CXCR4 pathway regulated osteosarcoma cells proliferation, migration and reduced apoptosis. Besides, we demonstrated that miR-613 was significantly downregulated in osteosarcoma patients. Elevated expression of miR-613 directly suppressed CXCR4 expression and then decreased the proliferation, migration and induced apoptosis of osteosarcoma cells. Moreover, our study found that CXCR4 promoted the development of lung metastases and inhibition of CXCR4 by miR-613 reduced lung metastases. These data indicated that CXCR4 mediated osteosarcoma cell growth and lung metastases and this effect can be suppressed by miR-613 through directly downregulating CXCR4.

| S-EPMC6113448 | biostudies-literature

MicroRNA-610 suppresses osteosarcoma oncogenicity via targeting TWIST1 expression.

Project description:Osteosarcoma is the most frequent primary bone tumor affects adolescents and young adults. Recently, microRNAs (miRNAs) are short, non-coding and endogenous RNAs that played as important roles in the initiation and progression of tumors. In this study, we try to explore the biological function and expression of miR-610 in the osteosarcoma. We showed that miR-610 expression was downregulated in the osteosarcoma tissues and cell lines. Elevated expression of miR-610 suppressed the osteosarcoma cell proliferation, cell cycle, invasion and EMT program. Moreover, overexpression of miR-610 increased sensitivity of MG-63 and U2OS cells to cisplatin. Twist1 was identified as a direct target gene of miR-610 in the osteosarcoma cell. Furthermore, we demonstrated that Twist1 was upregulated in the osteosarcoma tissues and cell lines. The expression of Twist1 was negatively associated with the expression of miR-610 expression in the osteosarcoma tissues. Ectopic expression of Twist1 inhibited the sensitivity of miR-610-overexpressing MG-63 cells to cisplatin. We also showed that overexpression of Twist1 increased the proliferation and invasion of miR-610-overexpressing MG-63 cells. These data indicated that ectopic expression of miR-610 suppressed the osteosarcoma cell proliferation, cell cylce, invasion and increased the sensitivity of osteosarcoma cells to cisplatin through targeting the Twist1 expression.

| S-EPMC5593553 | biostudies-literature

Long non-coding RNA NR2F1-AS1 promoted proliferation and migration yet suppressed apoptosis of thyroid cancer cells through regulating miRNA-338-3p/CCND1 axis.

Project description:Thyroid cancer (TC) is a prevalent endocrine malignant cancer whose pathogenic mechanism remains unclear. The aim of the study was to investigate the roles of long non-coding RNA (lncRNA) NR2F1-AS1/miRNA-338-3P/CCND1 axis in TC progression. Differentially expressed lncRNAs and mRNAs in TC tissues were screened out and visualized by R program. Relative expression of NR2F1-AS1, miRNA-338-3p and cyclin D1 (CCND1) was determined by quantitative real time polymerase chain reaction. In addition, Western blot analysis was adopted for evaluation of protein expression of CCND1. Targeted relationships between NR2F1-AS1 and miRNA-338-3p, as well as miRNA-338-3p and CCND1 were predicted using bioinformatics analysis and validated by dual-luciferase reporter gene assay. Besides, tumour xenograft assay was adopted for verification of the role of NR2F1-AS1 in TC in vivo. NR2F1-AS1 and CCND1 were overexpressed, whereas miRNA-338-3p was down-regulated in TC tissues and cell lines. Down-regulation of NR2F1-AS1 and CCND1 suppressed proliferation and migration of TC cells yet greatly enhanced cell apoptotic rate. Silence of NR2F1-AS1 significantly suppressed TC tumorigenesis in vivo. NR2F1-AS1 sponged miRNA-338-3p to up-regulate CCND1 expression to promote TC progression. Our study demonstrated that up-regulation of NR2F1-AS1 accelerated TC progression through regulating miRNA-338-3P/CCND1 axis.

| S-EPMC6714216 | biostudies-literature

Mesenchymal stem cell-derived exosomes carrying microRNA-150 suppresses the proliferation and migration of osteosarcoma cells via targeting IGF2BP1.

Project description:BackgroundMicroRNA-150 (miR-150) plays a critical role in varied types of human cancers. In this study, we explored the effect and mechanism of mesenchymal stem cell (MSC)-derived exosomes (exo) carrying miR-150 (MSC-Exo-150) on the proliferation, migration, invasion, and apoptosis of osteosarcoma (OS) cells.MethodsMiR-150 expression in OS cell lines was assessed by quantitative reverse-transcription PCR (qRT-PCR). MSCs were transfected with cell-miR-67 or has-miR-150, and grouped as MSC-67 or MSC-150. Exosomes were isolated from each group, and separately named MSC-Exo-67, MSC-Exo-150 and MSC-Exo. MTT or flow cytometry assay was used to analyze the proliferation or apoptosis of U2SO and HOS cells, respectively. Wound healing or transwell assay was utilized to examine the migration or invasion of U2SO and HOS cells, respectively. The target relationship of miR-150 and insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) was established using StarBase2.0 and verified by dual-luciferase reporter gene analysis. Xenografted tumor model was established in rats to confirm the inhibitory effect of MSC-Exo-150 on the growth of xenografted tumor in vivo.ResultsThe expression of miR-150 was downregulated in OS cell lines, and significantly higher in MSC-150 cells than that in MSCs. MiR-150 was overexpressed in MSC-Exo-150 group compared with MSC-Exo group. After transfection of MSC-Exo-150 into U2SO and HOS cells, cell viability, mobility and invasion rate were decreased, and the cell apoptosis was increased. MiR-150 targeted IGF2BP1 and IGF2BP1 expression was negatively modulated by miR-150. Overexpression of IGF2BP1 reversed the anti-tumor effect of MSC-Exo-150 on HOS cells.ConclusionsMSC-Exo-150 inhibited proliferation, migration, invasion, and induced apoptosis of OS cells by targeting IGF2BP1.

| S-EPMC8798822 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data