Analysis of circular RNA‑associated competing endogenous RNA network in breast cancer

Wang, Xuekang; Dong, Yanhan; Wu, Qiong; Lu, Tong; Wang, Yuanyong; Li, Wenchao; Liu, Chengyu; Xu, Wu

doi:10.3892/ol.2020.11247

Cited by 3 publications

(3 citation statements)

References 79 publications

(85 reference statements)

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“…Partly in line with our study, IL-20 aggravated AH through activation of ERK/p38MAPK/NRF2 signaling pathways [ 33 ]. More importantly, crRNA networks (circRNA-miRNA-mRNA) have been widely constructed for disease and cancer treatment [ 34 ]. With the documents discussed above, we believed that 1700020I14Rik could suppress miR-137 expression, which activates AKR1B10-Erk pathway in AH.…”

Section: Discussionmentioning

confidence: 99%

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

Bai

et al. 2022

Cell Death Discov.

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Alcoholic hepatitis (AH), a kind of alcoholic liver disease, shows poor prognosis. Long noncoding RNAs (lncRNAs) exert critical role in liver diseases. Here, we intended to investigate the possible molecular mechanism that 1700020I14Rik-based regulation of microRNA (miR)-137/Aldo-keto reductase family 1 member B10 (AKR1B10) affecting the inflammatory response and hepatocyte damage in AH. AH-related genes and the down-stream regulatory pathway were screnned by bioinformatics. Mouse normal hepatocyte cell line AML12 was selected to construct an ethanol-induced hepatocyte injury model for in vitro mechanistic validation, while we also established an AH mouse model using the ethanol with gradually increased concentration of 2–4% (v/v) for in vivo study. Specific role of 1700020I14Rik/miR-137/AKR1B10 in AML12 cell viability, proliferation and apoptotic capacity as well as inflammation and liver damage in mice were analyzed following ectopic and depletion approaches. We found elevated AKR1B10 and 1700020I14Rik but reduced miR-137 in AH. 1700020I14Rik was able to elevated miR-137-mediated AKR1B10. In vitro cell experiments and in vivo animal experiments validated that 1700020I14Rik reduced ethanol-induced hepatocyte damage and inflammation in AH mice through regulation of miR-137–mediated AKR1B10/Erk axis. The current study underlied that 1700020I14Rik could activate AKR1B10/Erk signaling through inhibition of miR-137, thereby promoting the hepatocyte damage in AH mice.

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Section: Discussionmentioning

confidence: 99%

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

Bai

et al. 2022

Cell Death Discov.

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“…Moreover, comprehensive transcriptomic analysis was performed to decipher ceRNA regulatory networks in endocrine-resistant breast cancer [ 18 ]. Additionally, the circular RNA-miRNA-mRNA networks involved in the tumorigenesis of breast cancer have been explored [ 19 ]. However, the molecular targets identified by bioinformatics analyses in these studies often lack validation experiments, and their functions in the biology of breast cancer should be further explored.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA MEG3 acts as a suppressor in breast cancer by regulating miR-330/CNN1

Yi,

Wang,

Yang

et al. 2024

Aging

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Background: The current study aimed to investigate the molecular mechanism of long non-coding RNA (lncRNA) MEG3 in the development of breast cancer. Methods: The regulating relationships among lncRNA MEG3, miRNA-330 and CNN1 were predicted by bioinformatics analysis of breast cancer samples in the Cancer Genome Atlas database. The differential expression of lncRNA MEG3, miRNA-330 and CNN1 was first validated in breast cancer tissues and cells. The effects of lncRNA MEG3 on breast cancer malignant properties were evaluated by manipulating its expression in MCF-7 and BT-474 cells. Rescue experiments, dual-luciferase assays, and RNA immunoprecipitation (RIP) experiments were further used to validate the relationships among lncRNA MEG3, miRNA-330 and CNN1. Results: Bioinformatics analysis showed that lncRNA MEGs and CNN1 were significantly downregulated in breast cancer tissues, while miR-330 was upregulated. These differential expressions were further validated in our cohort of breast cancer samples. High expression levels of lncRNA MEG3 and CNN1 as well as low expression of miR-330 were significantly associated with favorable overall survival. Overexpression of lncRNA MEG3 significantly inhibited cell viability, migration and invasion, decreased cells in S stage and promoted cell apoptosis. Dual-luciferase reporter gene assay and RIP experiments showed that lncRNA MEG3 could directly bind to miR-330. Moreover, miR-330 mimics on the basis of lncRNA MEG3 overexpression ameliorated the tumor-suppressing effects of lncRNA MEG3 in breast cancer malignant properties by decreasing CNN1 expression. Conclusion: Our study indicated lncRNA MEG3 is a breast cancer suppressor by regulating miR-330/CNN1 axis.

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“…Salmena et al (2011) proposed that molecules can play the regulatory role of competing endogenous RNA (ceRNA) by competing with the same microRNA (miRNA) response elements (Salmena et al, 2011). The ceRNA hypothesis states that miRNAs can regulate multiple target genes, and the same target genes can be regulated by different miRNAs (Wang and Liu, 2017). One hypothesis of ceRNA suggests that lncRNAs can sponge and inactivate miRNAs, ultimately reducing mRNA degradation or silencing mRNA translation, thus affecting protein coding (Salmena et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

ceRNA Network Analysis Shows That lncRNA CRNDE Promotes Progression of Glioblastoma Through Sponge mir-9-5p

Luo

Zhong

et al. 2021

Front. Genet.

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Glioblastoma accounts for 45.2% of central nervous system tumors. Despite the availability of multiple treatments (e.g., surgery, radiotherapy, chemotherapy, biological therapy, immunotherapy, and electric field therapy), glioblastoma has a poor prognosis, with a 5-year survival rate of approximately 5%. The pathogenesis and prognostic markers of this cancer are currently unclear. To this end, this study aimed to explore the pathogenesis of glioblastoma and identify potential prognostic markers. We used data from the GEO and TCGA databases and identified five genes (ITGA5, MMP9, PTPRN, PTX3, and STX1A) that could affect the survival rate of glioblastoma patients and that were differentially expressed between glioblastoma patients and non-tumors groups. Based on a variety of bioinformatics tools for reverse prediction of target genes associated with the prognosis of GBM, a ceRNA network of messenger RNA (STX1A, PTX3, MMP9)-microRNA (miR-9-5p)-long non-coding RNA (CRNDE) was constructed. Finally, we identified five potential therapeutic drugs (bacitracin, hecogenin, clemizole, chrysin, and gibberellic acid) that may be effective treatments for glioblastoma.

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Analysis of circular RNA‑associated competing endogenous RNA network in breast cancer

Cited by 3 publications

References 79 publications

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

LncRNA 1700020I14Rik promotes AKR1B10 expression and activates Erk pathway to induce hepatocyte damage in alcoholic hepatitis

Long non-coding RNA MEG3 acts as a suppressor in breast cancer by regulating miR-330/CNN1

ceRNA Network Analysis Shows That lncRNA CRNDE Promotes Progression of Glioblastoma Through Sponge mir-9-5p

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