Dataset Information

Long Non-Coding RNA LINC00511 Mediates the Effects of ESR1 on Proliferation and Invasion of Ovarian Cancer Through miR-424-5p and miR-370-5p.

ABSTRACT: Introduction:Estrogen receptor 1 (ESR1) plays an important role in the pathological events of ovarian cancer (OV), but the underlying mechanism is not completely understood. Using bioinformatics analysis, we found that ESR1 is involved in the regulation of some lncRNAs that are highly expressed in ovarian cancer. The lncRNAs might mediate the roles of ESR1 in OV occurrence and progression. Methods:This study measured the expression of the lncRNAs in OV cell lines using qRT-PCR. Some of the lncRNAs were silenced or overexpressed to determine their effects on the growth and invasion of CAOV3 cells with the stimulation of 17 beta-estradiol or not. Results:ESR1-expressing OV cells (CAOV3 cells) shows higher LINC00511 and RP11-166P13.3 expression than the ESR1-losing OV cells (UWB1.289 cells). Depletion of the two lncRNAs enhanced cell viability and invasion and decreased apoptosis rate. In these respects, effects of LINC00511 were more remarkable than that those of RP11-166P13.3. Treatment with 17 beta-estradiol to stimulate ESR1 increased LINC00511 expression, while ESR1 inhibitor Fulvestrant decreased LINC00511 expression. FISH assay confirmed that LINC00511 is present in the cytoplasm and nucleus. Bioinformatics analysis revealed the interaction of LINC00511 with miR-424-5p and miR-370-5p, which was further identified by RNA-pull down assay. As indicated by RIP assay, silencing LINC00511 increased the interaction between Ago protein and these two miRNAs. Discussion:Our study showed that ESR1-induced upregulation of LINC00511 promoted proliferation and invasion of CAOV3 cells probably through sponging miR-424-5p and miR-370-5p.

SUBMITTER: Wang K

PROVIDER: S-EPMC6938182 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Long Non-Coding RNA LINC00511 Mediates the Effects of ESR1 on Proliferation and Invasion of Ovarian Cancer Through miR-424-5p and miR-370-5p.

Wang Kang K Zhu Genhai G Bao Shan S Chen Shiling S

Cancer management and research 20191227

<h4>Introduction</h4>Estrogen receptor 1 (ESR1) plays an important role in the pathological events of ovarian cancer (OV), but the underlying mechanism is not completely understood. Using bioinformatics analysis, we found that ESR1 is involved in the regulation of some lncRNAs that are highly expressed in ovarian cancer. The lncRNAs might mediate the roles of ESR1 in OV occurrence and progression.<h4>Methods</h4>This study measured the expression of the lncRNAs in OV cell lines using qRT-PCR. So ...[more]

PMID: 31920390

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Project description:ObjectivesDeoxyelephantopin (DET) is a kind of natural active ingredient extracted from the Chinese herbal medicine Elephantopus scaber L. Many studies have revealed the potential antitumor effect on multiple malignancies. However, the detailed mechanism of its antitumor effect in pancreatic cancer remains unclear. Recently, studies have confirmed that noncoding RNA (ncRNA) plays an important regulatory role in malignancies. This research was performed to explore the relationship between ncRNA and DET-induced tumor inhibition in pancreatic cancer.MethodsMicroarray profiling was applied to identify the candidate ncRNAs associated with DET-induced tumor inhibition. Quantitative real-time PCR was used to evaluate the expression of linc00511 in pancreatic cancer cells and tissues. The influence of DET on the cell proliferation, migration, and invasion was assessed by CCK-8, colony formation, wound healing, and Transwell assays. The relationship between lncRNAs, miRNAs, and p21 promoter region was analyzed by bioinformatics and verified by luciferase reporter gene and western blotting. The effect of linc00511 on nuclear translocation of miR-370-5p was explored by cytoplasmic and nuclear RNA purification. Moreover, the effect of DET on tumor growth and metastasis, and the prophylactic effect were investigated by establishing subcutaneous and lung metastatic tumor models.ResultsMicroarray assay indicated linc00511 was a potential target gene. The antitumor effect of DET in pancreatic cancer depended on downregulating linc00511 expression, and linc00511 might be an oncogene in pancreatic cancer. Silencing linc00511 enhanced the antitumor function of DET; conversely, linc00511 overexpression antagonized the DET cytotoxic effect. Additionally, miR-370-5p could bind to p21 promoter to exert the RNA activation and then promote p21 expression. P21 was a downstream gene of linc00511 and associated with pancreatic cancer progression. Linc00511 regulated p21 expression by blocking miR-370-5p nuclear translocation.ConclusionsTo sum up, the present finding confirmed that DET suppressed the malignant biological behavior of pancreatic cancer via linc00511/miR-370-5p/p21 promoter axis.

Project description:BackgroundA loss of muscle mass occurs as a consequence of a range of chronic and acute diseases as well as in older age. This wasting results from an imbalance of protein synthesis and degradation with a reduction in synthesis and resistance to anabolic stimulation often reported features. Ribosomes are required for protein synthesis, so changes in the control of ribosome synthesis are potential contributors to muscle wasting. MicroRNAs (miRNAs) are known regulators of muscle phenotype and have been shown to modulate components of the protein synthetic pathway. One miRNA that is predicted to target a number of components of protein synthetic pathway is miR-424-5p, which is elevated in the quadriceps of patients with chronic obstructive pulmonary disease (COPD).MethodsTargets of miR-424-5p were identified by Argonaute2 pull down, and the effects of the miRNA on RNA and protein expression were determined by quantitative polymerase chain reaction and western blotting in muscle cells in vitro. Protein synthesis was determined by puromycin incorporation in vitro. The miRNA was over-expressed in the tibialis anterior muscle of mice by electroporation and the effects quantified. Finally, quadriceps expression of the miRNA was determined by quantitative polymerase chain reaction in patients with COPD and intensive care unit (ICU)-acquired weakness and in patients undergoing aortic surgery as well as in individuals from the Hertfordshire Sarcopenia Study.ResultsPull-down assays showed that miR-424-5p bound to messenger RNAs encoding proteins associated with muscle protein synthesis. The most highly enriched messenger RNAs encoded proteins required for the Pol I RNA pre-initiation complex required for ribosomal RNA (rRNA) transcription, (PolR1A and upstream binding transcription factor). In vitro, miR-424-5p reduced the expression of these RNAs, reduced rRNA levels, and inhibited protein synthesis. In mice, over-expression of miR-322 (rodent miR-424 orthologue) caused fibre atrophy and reduced upstream binding transcription factor expression and rRNA levels. In humans, elevated miR-424-5p associated with markers of disease severity in COPD (FEV1 %), in patients undergoing aortic surgery (LVEF%), and in patients with ICU-acquired weakness (days in ICU). In patients undergoing aortic surgery, preoperative miR-424-5p expression in skeletal muscle was associated with muscle loss over the following 7 days.ConclusionsThese data suggest that miR-424-5p regulates rRNA synthesis by inhibiting Pol I pre-initiation complex formation. Increased miR-424-5p expression in patients with conditions associated with muscle wasting is likely to contribute to the inhibition of protein synthesis and loss of muscle mass.

Dataset Information

Long Non-Coding RNA LINC00511 Mediates the Effects of ESR1 on Proliferation and Invasion of Ovarian Cancer Through miR-424-5p and miR-370-5p.

Publications

Long Non-Coding RNA LINC00511 Mediates the Effects of ESR1 on Proliferation and Invasion of Ovarian Cancer Through miR-424-5p and miR-370-5p.

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