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The lncRNA XIST regulates the tumorigenicity of renal cell carcinoma cells via the miR-302c/SDC1 axis.

ABSTRACT: Long non-coding RNAs (LncRNAs) are thought to be involved in several biological processes in carcinomas. The aim of this study is to evaluate the roles of lncRNA-XIST in the tumorigenicity of renal cell carcinoma (RCC) cells via the miR-302c/SDC1 axis. In this study, the expression levels of miR-302c and XIST in RCC tissues and cells were analyzed by qRT-PCR. Cell proliferation was measured using MTT and colony formation assays, and cell apoptosis was detected using flow cytometry. The interaction between XIST and miR-302c was analyzed using a luciferase reporter gene assay. RCC tissues and cells exhibited decreased miR-302c expression and increased lncRNA-XIST expression. Furthermore, XIST negatively regulated miR-302c by directly binding regulatory sites in RCC cells. In addition, XIST silencing with siRNAs significantly inhibited the proliferation and promoted the apoptosis of 786-O and Caki-1 cells. Knockdown of Syndecan-1 (SDC1), a miR-302c target gene, yielded similar results as XIST silencing. In summary, XIST regulated the development and progression of RCC by inhibiting the miR302c/SDC1 axis.

SUBMITTER: Zhang J

PROVIDER: S-EPMC6965219 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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The lncRNA XIST regulates the tumorigenicity of renal cell carcinoma cells via the miR-302c/SDC1 axis.

Zhang Jianglei J Cao Zhijun Z Ding Xiang X Wei Xuedong X Zhang Xuefeng X Hou Jianquan J Ouyang Jun J

International journal of clinical and experimental pathology 20170701 7

Long non-coding RNAs (LncRNAs) are thought to be involved in several biological processes in carcinomas. The aim of this study is to evaluate the roles of lncRNA-XIST in the tumorigenicity of renal cell carcinoma (RCC) cells via the miR-302c/SDC1 axis. In this study, the expression levels of miR-302c and XIST in RCC tissues and cells were analyzed by qRT-PCR. Cell proliferation was measured using MTT and colony formation assays, and cell apoptosis was detected using flow cytometry. The interacti ...[more]

PMID: 31966592

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Project description:Background: Vascular aging is considered a special risk factor for cardiovascular diseases, and vascular smooth muscle cells (VSMCs) play a major role in aging-related vascular remodeling and in the pathological process of atherosclerosis. Recent research has reported that long non-coding RNA/microRNA (lncRNA/miRNA) is a critical regulator of cellular senescence. However, the role and mechanism of lncRNA GAS5/miR-665 axis in VSMC senescence remain incompletely understood. Methods: Cellular senescence was evaluated using senescence-associated β-gal activity, the NAD+/NADH ratio, and by immunofluorescence staining of γH2AX immunofluorescence. Differentially expressed miRNAs (DEMs) were identified by miRNA microarray assays and subsequently validated by quantitative real-time PCR (qRT-PCR). A dual luciferase reporter assay was conducted to confirm the binding of lncRNA GAS5 and miR-665 as well as miR-665 and syndecan 1 (SDC1). Serum levels of miR-665, lncRNA GAS5, and SDC1 in 93 subjects were detected by qRT-PCR. The participants were subdivided into control, aging, and early vascular aging (EVA) groups, and their brachial-ankle pulse wave velocity (baPWV) was measured. Results: A total of 20 overlapping DEMs were identified in young and old VSMCs via microarray analysis. MiR-665 showed a significant alteration and, therefore, was selected for further analysis. Upregulation of miR-665 was found in aging VSMCs, and downregulation of miR-665 caused an inhibition of VSMCs senescence. Subsequently, the dual luciferase reporter assay determined the binding site of miR-665 with the 3'-UTR of lncRNA GAS5 and SDC1. Increased expression of lncRNA GAS5 expression inhibited the miR-665 level and VSMC senescence. However, as shown in rescue experiment results, either miR-665 overexpression or SDC1 knockdown significantly reversed the effects of lncRNA GAS5 on VSMC senescence. Finally, compared with that of the control group, miR-665 was highly expressed in serum samples in the aging and EVA groups, especially in the EVA groups. On the contrary, serum levels of lncRNA GAS5 and SDC1 were lower in these two groups. Collectively, in the aging and EVA groups, miR-665 expression was negatively correlated with lncRNA GAS5 and SDC1 expression. Conclusion: miR-665 inhibition functions as a vital modulator of VSMC senescence by negatively regulating SDC1, which is achieved by lncRNA GAS5 that sponges miR-665. Our findings may provide a new treatment strategy for aging-related cardiovascular diseases.

Project description:BackgroundNeuroinflammation is a common feature of many neurological diseases, and remains crucial for disease progression and prognosis. Activation of microglia and astrocytes can lead to neuroinflammation. However, little is known about the role of lncRNA xist and miR-122-5p in the pathogenesis of sepsis-associated neuroinflammation (SAN). This study aims to investigate the role of lncRNA xist and miR-122-5p in the pathogenesis of SAN.MethodsLevels of miR-122-5p and proinflammatory mediators were detected in the cerebrospinal fluid (CSF) of patients with intracranial infection (ICI) by ELISA and qRT-PCR. miRNA expression in the periventricular white matter (PWM) in rats was analyzed by high-throughput sequencing. Levels of lncRNA xist, miR-122-5p and proinflammatory mediators in the PWM were measured using qRT-PCR and western blot. Bioinformatics analysis was used to predict the upstream and downstream of miR-122-5p. The interaction between miR-122-5p and its target protein was validated using luciferase reporter assay. BV2 and astrocytes were used to detect the expression of lncRNA xist, miR-122-5p.ResultsThe level of miR-122-5p was significantly decreased in the CSF of ICI patients, while the expression of IL-1β and TNF-α were significantly upregulated. Furthermore, it was found that the expression of IL-1β and TNF-α were negatively correlated with the level of miR-122-5p. A high-throughput sequencing analysis showed that miR-122-5p expression was downregulated with 1.5-fold changes in the PWM of CLP rats compared with sham group. Bioinformatics analysis found that lncRNA xist and PKCη were the upstream and downstream target genes of miR-122-5p, respectively. The identified lncRNA xist and PKCη were significantly increased in the PWM of CLP rats. Overexpression of miR-122-5p or knockdown of lncRNA xist could significantly downregulate the level of PKCη and proinflammatory mediators from activated microglia and astrocytes. Meanwhile, in vitro investigation showed that silencing lncRNA xist or PKCη or enhancing the expression of miR-122-5p could obviously inhibit the release of proinflammatory mediators in activated BV2 cells and astrocytes.ConclusionLncRNA xist could regulate microglia and astrocytes activation in the PWM of CLP rats via miR-122-5p/PKCη axis, further mediating sepsis associated neuroinflammation.

Dataset Information

The lncRNA XIST regulates the tumorigenicity of renal cell carcinoma cells via the miR-302c/SDC1 axis.

Publications

The lncRNA XIST regulates the tumorigenicity of renal cell carcinoma cells via the miR-302c/SDC1 axis.

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