Long non-coding RNA OIP5-AS1 promotes the progression of esophageal cancer by regulating miR-30a/VOPP1 expression.
Ontology highlight
ABSTRACT:
SUBMITTER: Xu J
PROVIDER: S-EPMC8299025 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Numerous studies have suggested that dysregulated long noncoding RNAs (lncRNAs) contributed to the development and progression of many cancers. lncRNA OIP5 antisense RNA 1 (OIP5-AS1) has been reported to be increased in several cancers. However, the roles of OIP5-AS1 in liver hepatocellular carcinoma (LIHC) remain to be investigated. In this study, we demonstrated that OIP5-AS1 was upregulated in LIHC tissue specimens and its overexpression was associated with the poor survival of patients with LIHC. Furthermore, loss-of function experiments indicated that OIP5-AS1 promoted cell proliferation and inhibited cell apoptosis both in vitro and in vivo. Moreover, binding sites between OIP5-AS1 and hsa-miR-26a-3p as well as between hsa-miR-26a-3p and EPHA2 were confirmed by luciferase assays. Finally, a rescue assay was performed to prove the effect of the OIP5-AS1/hsa-miR-26a-3p/EPHA2 axis on LIHC cell biological behaviors. Based on all of the above findings, our results suggested that OIP5-AS1 promoted LIHC cell proliferation and invasion via regulating the hsa-miR-26a-3p/EPHA2 axis.
| S-EPMC7321793 | biostudies-literature
Project description:Breast cancer is the most common invasive cancer in women with the highest number of related deaths which is caused by distal metastasis. Recently, integrated analysis of gene expression profile suggested widespread gene dysregulation in various types of cancer. Research in the past decade has focused on long non?coding RNAs (lncRNAs), particularly in cell proliferation, tumor progression and metastasis. OPA?interacting protein 5 antisense transcript 1 (OIP5?AS1) is an evolutionarily conserved long non?coding RNA that has been linked to oncogenesis in multiple cancers. In breast cancer, dysregulation of OIP5?AS1 was reported but the precise role in cancer development and progression remains unclear. In the present study, using small interfering RNA (siRNA) targeting OIP5?AS1, it was shown that knockdown of OIP5?AS1 was associated with alteration of EMT markers and suppressed migration and invasion of breast cancer cells. Among the EMT?related transcription factors, ZEB1 and ZEB2 were significantly downregulated with OIP5?AS1 knockdown. Computational analysis and a dual?luciferase reporter system identified miR?340?5p was the target gene for OIP5?AS1. Further experiments verified the function of OIP5?AS1 in cell invasion was dependent on miR?340a?5p through regulating target gene ZEB2. In vivo study demonstrated that overexpressing OIP5?AS1 in breast cancer cells promoted lung metastasis in nude mice. The findings of the present study revealed the mechanism of OIP5?AS1 in breast cancer metastasis. Overall, our study may provide a potential therapeutic target for breast cancer metastasis.
| S-EPMC7448425 | biostudies-literature
Project description:Background:Multiple myeloma (MM) is a prevalent hematological malignancy. Long noncoding RNAs are correlated with the development of MM. In this project, the function of lncRNA opa interacting protein 5-antisense 1 (OIP5-AS1) in MM and the potential mechanistic pathway were explored. Methods:The expression of OIP5-AS1, microRNA (miR)-27a-3p and tuberous sclerosis 1 (TSC1) was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and Bromodeoxyuridine (BrdU) staining. And cell apoptosis was evaluated by flow cytometry assay. Cell metastasis was assessed utilizing transwell assay. Western blot analysis was employed to detect protein level. The target relation between miR-27a-3p and OIP5-AS1 or TSC1 was confirmed via dual-luciferase reporter assay and RNA immunoprecipitation assay. Tumor xenograft assay was conducted to measure the function of OIP5-AS1 in vivo. Results:The expression levels of OIP5-AS1 and TSC1 were decreased in MM, whereas miR-27a-3p was upregulated. High level of OIP5-AS1 could predict favourable prognosis of MM patients. Overexpression of OIP5-AS1 inhibited cell viability, colony formation ability, migration and invasion, induced cell cycle arrest in G1 phase and apoptosis of MM cells in vitro as well as repressed tumorigenesis in vivo. MiR-27a-3p was a target of OIP5-AS1, and reversed the impact of OIP5-AS1 on MM cells. MiR-27a-3p directly targeted TSC1. Silencing of miR-27a-3p repressed MM progression by elevating TSC1 expression. OIP5-AS1 upregulated TSC1 by sponging miR-27a-3p. Conclusion:OIP5-AS1 repressed multiple myeloma progression by regulating miR-27a-3p/TSC1 axis.
| S-EPMC7206794 | biostudies-literature
Project description:Long non‑coding RNA (LncRNA) o‑phthalaldehyde-interacting protein 5 antisense transcript 1 (OIP5‑AS1) serves major roles in the progression of various types of cancer. The present study investigated its biological function in ovarian cancer (OC) and its mechanisms. The levels of OIP5‑AS1, microRNA‑128‑3p (miR‑128‑3p) and cyclin G1 (CCNG1) were examined by reverse transcription‑quantitative PCR. Cell viability, apoptosis, migration and invasion were detected to analyze cellular progression. Glycolytic metabolism was assessed by detecting the levels of glucose consumption and lactate production. CCNG1 and hexokinase 2 protein levels were measured by western blotting. Dual‑luciferase reporter assay, RNA immunoprecipitation and RNA pull‑down assays were performed to affirm the interaction between two molecules. OIP5‑AS1 was found to be upregulated in OC tissues and cells. Knockdown of OIP5‑AS1 suppressed cell viability, migration, invasion and glycolysis while promoting apoptosis in OC cells. OIP5‑AS1 interacted with miR‑128‑3p and functioned as an oncogene by sequestering miR‑128‑3p. In addition, CCNG1 was a target gene for miR‑128‑3p and miR‑128‑3p regulated the CCNG1‑induced effects on OC cells by downregulating CCNG1. OIP5‑AS1 upregulated the expression of CCNG1 via targeting miR‑128‑3p. OIP5‑AS1 knockdown also inhibited tumor growth of OC in vivo by modulating the expression of miR‑128‑3p and CCNG1. Collectively, these data illustrated that the oncogenic role of OIP5‑AS1 in OC was associated with the miR‑128‑3p/CCNG1 axis at least in part. OIP5‑AS1 might be a probable diagnostic and therapeutic biomarker for the treatment of OC patients.
| S-EPMC8008222 | biostudies-literature
Project description:An increasing number of studies have shown that long non‑coding RNAs (lncRNAs) are crucially involved in tumorigenesis. However, the biological functions, underlying mechanisms and clinical value of lncRNA PC‑esterase domain containing 1B‑antisense RNA 1 (PCED1B‑AS1) in pancreatic ductal adenocarcinoma (PDAC) have not been determined, to the best of our knowledge. In the present study, the expression of PCED1B‑AS1, microRNA (miR)‑411‑3p and hypoxia inducible factor (HIF)‑1α mRNA in 47 cases of PDAC tissues were detected using reverse transcription‑quantitative (RT‑q)PCR. Moreover, the effects of PCED1B‑AS1 on the biological behaviors of PDAC cells were assessed using Cell Counting Kit‑8, EdU staining and Transwell assays. Bioinformatics analysis, RT‑qPCR, western blotting, dual luciferase reporter gene and RNA immunoprecipitation assays were performed to determine the regulatory relationships between PCED1B‑AS1, miR‑411‑3p and HIF‑1α. We demonstrated that PCED1B‑AS1 was significantly upregulated in PDAC tumor tissues, and its expression was associated with advanced Tumor‑Node‑Metastasis stage and lymph node metastasis. PCED1B‑AS1 knockdown inhibited PDAC cell proliferation, invasion as well as epithelial‑mesenchymal transition (EMT) in vitro. Mechanistically, PCED1B‑AS1 was shown to target miR‑411‑3p, resulting in the upregulation of HIF‑1α. In conclusion, PCED1B‑AS1 expression was upregulated in PDAC tissues and cells, and it participated in promoting the proliferation, invasion and EMT of cancer cells by modulating the miR‑411‑3p/HIF‑1α axis.
| S-EPMC8144929 | biostudies-literature
Project description:ObjectiveLong non-coding RNAs (lncRNAs) feature prominently in tumors. Reportedly, lncRNA zinc finger E-box-binding homeobox 2 antisense RNA 1 (ZEB2-AS1) is aberrantly expressed in a variety of tumors. The present study was aimed to explore ZEB2-AS1 functions and determine mechanism in hepatocellular carcinoma (HCC) progression.Materials and methodsIn this experimental study, expressions of ZEB2-AS1, microRNA (miR)-582-5p and forkhead box C1 (FOXC1) mRNA in HCC tissues and cell lines were detected via quantitative reveres transcription polymerase chain reaction (qRT-PCR). After establishing gain- and loss-of-functions models, cell counting kit-8, 5-bromo-2'-deoxyuridine (BrdU), Transwell assays and flow cytometry analysis were conducted to examine HCC cell multiplication, migration, invasion and apoptosis, respectively. The targeted relationship between miR-582- 5p and ZEB2-AS1 was verified via dual-luciferase reporter gene assay. Western blot was utilized for detecting FOXC1 expression in HCC cells after selectively regulating ZEB2-AS1 and miR-582-5p.ResultsIn HCC tissues and cells, ZEB2-AS1 expression was increased. High ZEB2-AS1 expression was related to relatively large tumor volume, increased tumor-node-metastasis (TNM) stage and positive lymph node metastasis of the patients. ZEB2-AS1 overexpression facilitated HCC cell multiplication, migration, invasion and suppressed apoptosis, while ZEB2-AS1 knock-down caused the opposite effects. It was also confirmed that ZEB2-AS1 could competitively bind with miR-582-5p to repress its expression, and indirectly up-regulate FOXC1 expression level in HCC cells.ConclusionThe current study revealed that ZEB2-AS1 was over-expressed in HCC tissues and cells. It also upregulated (FOXC1), through sponging miR-582-5p, to promote HCC progression. This provides new perspectives for elucidating the pathogenesis of HCC.
| S-EPMC9315215 | biostudies-literature
Project description:Objective:Long noncoding RNA (LncRNA) SBF2-AS1 was reportedly to function as an oncogene in several types of cancers, such as hepatocellular carcinoma, nonsmall cell lung cancer, glioma, and colorectal cancer. However, the biological roles and regulatory mechanisms of SBF2-AS1 in gastric cancer (GC) are unknown. Methods:The expression of SBF2-AS1 and miR-545 were examined in GC tissues and cell lines via real-time quantitative PCR. The relationship of SBF2-AS1 with miR-545 was verified via dual-luciferase reporter gene assay and RNA immunoprecipitation. The influences of SBF2-AS1 on cell proliferation, migration, and invasion were determined using cell counting Kit-8 (CCK-8), wound healing, and transwell invasion assays, respectively. Results:LncRNA SBF2-AS1 expression was upregulated in GC tissues, especially in advanced clinical stage cases. Moreover, increased SBF2-AS1 indicated a poor survival rate. Functionally, the downregulation of SBF2-AS1 by siRNA in GC cells suppressed the proliferation, migration, and invasion. In terms of mechanism, SBF2-AS1 can directly bind to miR-545 and regulate its expression. Moreover, SBF2-AS1 knockdown significantly decreased the expression of EMS1, which was the direct target of miR-545. Importantly, inhibition of miR-545 or overexpression of EMS1 partially reversed SBF2-AS1-depletion-caused suppression on proliferation, migration, and invasion. Conclusion:These findings elucidated a crucial role of SBF2-AS1 as a miR-545 sponge in GC cells, suggesting that SBF2-AS1 might be a potential target for GC.
| S-EPMC7306839 | biostudies-literature
Project description:BackgroundLong noncoding RNAs (lncRNAs) play essential roles in tumor progression. However, the functions and targets of lncRNAs in neuroblastoma (NB) progression still remain to be determined. In this study, we aimed to investigate the effect of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) on NB and the underlying mechanism involved.MethodsThrough mining of public microarray datasets, we identify aberrantly expressed lncRNAs in NB. The gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, wound-healing assay, transwell invasion assays and flow cytometry analysis were utilized to examine cell proliferation, migration, invasion and apoptosis. Luciferase reporter assay was performed to confirm the interaction between DLX6-AS1and its potential targets. Tumor xenograft assay was used to verify the role of DLX6-AS1 in NB in vivo.ResultsWe identified DLX6-AS1 was upregulated in NB by using a public microarray dataset. The expression of DLX6-AS1 was increased in NB tissues and derived cell lines, and high expression of DLX6-AS1 was positively correlated with advanced TNM stage and poor differentiation. Knockdown of DLX6-AS1 induced neuronal differentiation, apoptosis and inhibited the growth, invasion, and metastasis of NB cells in vitro and impaired tumor growth in vivo. MiR-107 was the downstream target of DLX6-AS1. MiR-107 was found to target brain-derived neurotrophic factor (BDNF) which is an oncogene in NB. Knockdown of miR-107 or overexpression of BDNF reversed the suppression of NB progression caused by DLX6-AS1 silence.ConclusionOverall, our finding supports that DLX6-AS1 promotes NB progression by regulating miR-107/BDNF pathway, acting as a novel therapeutic target for NB.
| S-EPMC6880520 | biostudies-literature
Project description:BackgroundPapillary thyroid cancer (PTC) is the most common type of cancer of the endocrine system. Long noncoding RNAs (lncRNAs) are emerging as a novel class of gene expression regulators associated with tumorigenesis. Through preexisting databases available for differentially expressed lncRNAs in PTC, we uncovered that lncRNA OIP5-AS1 was significantly upregulated in PTC tissues. However, the function and the underlying mechanism of OIP5-AS1 in PTC are poorly understood.MethodsExpression of lncRNA OIP5-AS1 and miR-98 in PTC tissue and cells were measured by quantitative real-time PCR (qRT-PCR). And expression of METTL14 and ADAMTS8 in PTC tissue and cells were measured by qRT-PCR and western blot. The biological functions of METTL14, OIP5-AS1, and ADAMTS8 were examined using MTT, colony formation, transwell, and wound healing assays in PTC cells. The relationship between METTL14 and OIP5-AS1 were evaluated using RNA immunoprecipitation (RIP) and RNA pull down assay. And the relationship between miR-98 and ADAMTS8 were examined by luciferase reporter assay. For in vivo experiments, a xenograft model was used to investigate the effects of OIP5-AS1 and ADAMTS8 in PTC.ResultsFunctional validation revealed that OIP5-AS1 overexpression promotes PTC cell proliferation, migration/invasion in vitro and in vivo, while OIP5-AS1 knockdown shows an opposite effect. Mechanistically, OIP5-AS1 acts as a target of miR-98, which activates ADAMTS8. OIP5-AS1 promotes PTC cell progression through miR-98/ADAMTS8 and EGFR, MEK/ERK pathways. Furthermore, RIP and RNA pull down assays identified OIP5-AS1 as the downstream target of METTL14. Overexpression of METTL14 suppresses PTC cell proliferation and migration/invasion through inhibiting OIP5-AS1 expression and regulating EGFR, MEK/ERK pathways.ConclusionsCollectively, our findings demonstrate that OIP5-AS1 is a METTL14-regulated lncRNA that plays an important role in PTC progression and offers new insights into the regulatory mechanisms underlying PTC development.
| S-EPMC8206147 | biostudies-literature
Project description:Rationale: Glioma is the most common primary malignant tumor of human central nervous system, and its rich vascular characteristics make anti-angiogenic therapy become a therapeutic hotspot. However, the existence of glioma VM makes the anti-angiogenic therapy ineffective. SUMOylation is a post-translational modification that affects cell tumorigenicity by regulating the expression and activity of substrate proteins. Methods: The binding and modification of IGF2BP2 and SUMO1 were identified using Ni2+-NTA agarose bead pull-down assays, CO-IP and western blot; and in vitro SUMOylation assays combined with immunoprecipitation and immunofluorescence staining were performed to explore the detail affects and regulations of the SUMOylation on IGF2BP2. RT-PCR and western blot were used to detect the expression levels of IGF2BP2, OIP5-AS1, and miR-495-3p in glioma tissues and cell lines. CCK-8 assays, cell transwell assays, and three-dimensional cell culture methods were used for evaluating the function of IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14 in biological behaviors of glioma cells. Meantime, RIP and luciferase reporter assays were used for inquiring into the interactions among IGF2BP2, OIP5-AS1, miR-495-3p, HIF1A and MMP14. Eventually, the tumor xenografts in nude mice further as certained the effects of IGF2BP2 SUMOylation on glioma cells. Results: This study proved that IGF2BP2 mainly binds to SUMO1 and was SUMOylated at the lysine residues K497, K505 and K509 sites, which can be reduced by SENP1. SUMOylation increased IGF2BP2 protein expression and blocked its degradation through ubiquitin-proteasome pathway, thereby increasing its stability. The expressions of IGF2BP2 and OIP5-AS1 were up-regulated and the expression of miR-495-3p was down-regulated in both glioma tissues and cells. IGF2BP2 enhances the stability of OIP5-AS1, thereby increasing the binding of OIP5-AS1 to miR-495-3p, weakening the binding of miR-495-3p to the 3'UTR of HIF1A and MMP14 mRNA, and ultimately promoting the formation of VM in glioma. Conclusions: This study first revealed that SUMOylation of IGF2BP2 regulated OIP5-AS1/miR-495-3p axis to promote VM formation in glioma cells and xenografts growth in nude mice, providing a new idea for molecular targeted therapy of glioma.
| S-EPMC8326132 | biostudies-literature