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Integrated functional ceRNA network analysis reveals that circLIPH promotes pancreatic cancer progression via the miR-769-3p/GOLM1/mTOR pathway

ABSTRACT: Integrated functional ceRNA network analysis reveals that circLIPH promotes pancreatic cancer progression via the miR-769-3p/GOLM1/mTOR pathway

PROVIDER: PRJNA1036633 | ENA |

REPOSITORIES: ENA

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Integrated functional ceRNA network analysis reveals that circLIPH promotes pancreatic cancer progression via the miR-769-3p/GOLM1/mTOR pathway

Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most common malignancy of the pancreas with a high mortality rate because of metastasis of advanced tumors and recurrence after treatment. To identify more informative detection, diagnostic, and prognostic markers for improving the clinical therapeutic outcome of PDAC patients, we employed an SBC ceRNA array to screen differentially expressed ceRNAs in PDAC tumors, and circRNA/lncRNA-miRNA-mRNA regulatory networks were constructed. Gain- and loss-of-function experiments were also conducted to verify the biological function of circLIPH in vitro and in vivo. We found that 145 mRNAs and 358 circRNAs were differentially expressed in PDAC tumors. High circLIPH expression was correlated with tumor size and stage, and the inhibition of circLIPH repressed pancreatic cancer progression. We identified that circLIPH promoted pancreatic cancer progression via the miR-769-3p/GOLM1/mTOR pathway and might be a key regulator of tumorigenesis in PDAC.

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Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.

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MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation.

2016-10-23 | GSE51689 | GEO

MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation.

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