miR-217 is an oncogene that enhances the germinal center reaction

Yébenes, Virginia G. de; Bartolomé-Izquierdo, Nahikari; Nogales-Cadenas, Rubén; Pérez-Durán, Pablo; Mur, Sonia M.; Martínez, Nerea; Lisio, Lorena Di; Robbiani, Davide F.; Pascual-Montano, Alberto; Cañamero, Marta; Piris, Miguel Á.; Ramiro, Almudena R.

doi:10.1182/blood-2013-12-543611

Cited by 53 publications

(39 citation statements)

References 58 publications

(72 reference statements)

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“…However, in another study of pancreatic ductal adenocarcinoma, miR-217 was reported to inhibit the functions of KRAS, the loss of which enhanced tumor proliferation [40]. By contrast, miR-217 was demonstrated to act as an oncogene in aggressive human B-cell lymphomas, and it down-regulated the expression of a DNA damage response and repair gene network and, in turn, stabilized Bcl-6 [41]. Considering these reported differences in a few types of cancers, we hypothesize that the role of miR-217 might be cancer species dependent and further investigations are required.…”

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

et al. 2017

Cell Physiol Biochem

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Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

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Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

et al. 2017

Cell Physiol Biochem

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“…Although miR-217 is overexpressed in aggressive human B-cell lymphomas and promotes mature B-cell lymphomagenesis [28], most studies suggest that miR-217 functions as a tumor suppressor in a variety of cancers. In pancreatic ductal adenocarcinoma, miR-217 inhibits tumor cell growth by targeting KRAS and SIRT1 [22, 37].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-217 inhibits clear cell renal cell carcinoma, hepatocellular carcinoma, gastric cancer and glioma by targeting E2F3, EZH2 and Runx2, respectively [24–27]. In contrast, miR-217 was proposed to be an oncogene by targeting PTEN, DACH1, PPARγ co-activator 1-α (PGC1-α) and enhances the germinal center reaction [28–31]. Based on these reports, it is attempting to speculate that miR-217 has context-dependent functions in carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

et al. 2017

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Triple negative breast cancer (TNBC) is one of the most aggressive breast cancers without effective targeted therapies. Numerous studies have implied that KLF5 plays an important roles in TNBC. How is KLF5 regulated by microRNAs has not been well studied. Here, we demonstrated that miR-217 down-regulates the expression of KLF5 and KLF5’s downstream target gene FGF-BP and Cyclin D1 in TNBC cell lines HCC1806 and HCC1937. Consequently, miR-217 suppresses TNBC cell growth, migration, and invasion. MiR-217 suppresses TNBC, at least partially, through down-regulating the KLF5 expression. These results suggest that the miR-217-KLF5 axis might serve as a potential target for treatment of TNBC.

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“…Previous studies have shown that miR-217 acts as a tumor suppressor by targeting the oncogene SirT1 in endothelial cells (13), while it also acts as an oncogene by targeting PTEN, a tumor suppressor gene, in kidney cells and by enhancing the germinal center (GC) reaction in GC B-cells (16,28). These findings prompted us to explore its expression and biological function in CRC.…”

Section: Discussionmentioning

confidence: 99%

miR-217 regulates tumor growth and apoptosis by targeting the MAPK signaling pathway in colorectal cancer

Zhang

Chen

2016

Oncology Letters

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MicroRNA (miR)-217 has been reported to participate in carcinogenesis and tumor progression in several cancers; however, its expression and biological functions in colorectal cancer (CRC) are still unclear. The present study demonstrated that miR-217 expression was significantly higher in matched adjacent noncancerous tissues than in CRC tissues (P<0.001). In addition, it was observed that low-grade CRC exhibited greater expression of miR-217 compared with high-grade CRC (P<0.05). Kaplan-Meier survival and Cox regression analyses revealed that overall survival rates were significantly poorer in the low-expression group relative to the high-expression group (P<0.005). Next, a potential miR-217 target, mitogen-activated protein kinase (MAPK) 1, was identified. Upregulation of miR-217 could significantly downregulate MAPK1 expression. CRC cells overexpressing miR-217 exhibited cell growth inhibition by significant enhancement of apoptosis in vitro. The present study further investigated the MAPK signaling pathway to verify the mechanisms, and revealed that KRAS and Raf-1 expression was downregulated in miR-217-overexpressing RKO cells. Taken together, our results revealed that miR-217 inhibits tumor growth and enhances apoptosis in CRC, and that this is associated with the downregulation of MAPK signaling. These results indicate that miR-217 is a promising therapeutic target for the treatment of CRC.

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miR-217 is an oncogene that enhances the germinal center reaction

Abstract: Key Points miR-217 enhances the GC reaction by dampening genotoxic-induced Bcl-6 degradation in GC B cells. miR-217 is an oncogene and its overexpression provides a model of miRNA-induced mature B-cell lymphomagenesis.

Cited by 53 publications

References 58 publications

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

miR-217 regulates tumor growth and apoptosis by targeting the MAPK signaling pathway in colorectal cancer

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