miR-188 Inhibits Glioma Cell Proliferation and Cell Cycle Progression Through Targeting β-Catenin

Li, Nan; Shi, Hangyu; Zhang, Lu; Li, Xu; Zhang, Gang; Shi, Yuanjie; Guo, Shiwen

doi:10.3727/096504017x15127309628257

Cited by 25 publications

(23 citation statements)

References 8 publications

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“…However, we performed a local blast with miR-188-5p sequence as query and CASC11 as target, but no promising target site of miR-188-5p was found on the sequence of CASC11. It is known that both CASC11 and miR-188-5p can interact with WNT/β-catenin [10,18]. Therefore, WNT/β-catenin may mediate the interaction between CASC11 and miR-188-5p in HCC.…”

Section: Discussionmentioning

confidence: 99%

LncRNA CASC11 promotes cancer cell proliferation in hepatocellular carcinoma by inhibiting miRNA-188-5p

Cheng

Yin

et al. 2019

Bioscience Reports

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It is known that lncRNA CASC11 promotes the development of gastric cancer. Our study was carried out to investigate the possible involvement of ncRNA CASC11 in hepatocellular carcinoma (HCC). In the present study, we found that CASC11 was up-regulated, while miR-188-5p was down-regulated in tumor tissues of HCC patients. CASC11 and miR-188-5p were not affected by HBV and HCV infections. Follow-up study showed that high levels of CASC11 were significantly correlated with poor survival. Expression levels of CASC11 and miR-188-5p were inversely correlated in tumor tissues. CASC11 overexpression mediated the down-regulation of miR-188-5p, while miR-188-5p overexpression failed to affect CASC11 expression. CASC11 overexpression led to promoted, while miR-188-5p overexpression led to inhibited proliferation of cells of HCC cell lines. CASC11 overexpression showed no significant effects on cancer cell migration and invasion. In addition, miR-188-5p overexpression attenuated the enhancing effects of CASC11 overexpression on cancer cell proliferation. Therefore, LncRNA CASC11 promoted cancer cell proliferation in HCC possibly by inhibiting miR-188-5p.

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Section: Discussionmentioning

confidence: 99%

LncRNA CASC11 promotes cancer cell proliferation in hepatocellular carcinoma by inhibiting miRNA-188-5p

Cheng

Yin

et al. 2019

Bioscience Reports

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“…Although not discussed by the authors, there was a tendency for higher expression levels of miR-9 and miR-188 in MCC samples. MiR-188 suppresses proliferation in different cancers [ 118 , 119 , 120 , 121 ]. MiR-9 can stimulate or inhibit cell proliferation and metastasis depending on the type of cancer, whereas high expression levels in most cancers are associated with poor survival of the patients, except for ovarian cancer patients, in which an inverse correlation was found [ 122 , 123 ].…”

Section: Merkel Cell Carcinoma and Micrornasmentioning

confidence: 99%

MicroRNAs as Potential Biomarkers in Merkel Cell Carcinoma

Konstantinell

Coucheron

Sveinbjørnsson

et al. 2018

IJMS

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Merkel cell carcinoma (MCC) is a rare and aggressive type of skin cancer associated with a poor prognosis. This carcinoma was named after its presumed cell of origin, the Merkel cell, which is a mechanoreceptor cell located in the basal epidermal layer of the skin. Merkel cell polyomavirus seems to be the major causal factor for MCC because approximately 80% of all MCCs are positive for viral DNAs. UV exposure is the predominant etiological factor for virus-negative MCCs. Intracellular microRNA analysis between virus-positive and virus-negative MCC cell lines and tumor samples have identified differentially expressed microRNAs. Comparative microRNA profiling has also been performed between MCCs and other non-MCC tumors, but not between normal Merkel cells and malignant Merkel cells. Finally, Merkel cell polyomavirus encodes one microRNA, but its expression in virus-positive MCCs is low, or non-detectable or absent, jeopardizing its biological relevance in tumorigenesis. Here, we review the results of microRNA studies in MCCs and discuss the potential application of microRNAs as biomarkers for the diagnosis, progression and prognosis, and treatment of MCC.

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“…Thereafter, miR-188 was reported to modulate cell senescence in bone marrow and suppress the proliferation and cell cycle in glioma. 23,24 Also, miR-188 played an important function in NPC. For example, Wu et al suggested that miR-188 inhibited G1/S transition through regulating cyclin/CDK axis in NPC cells.…”

Section: Introductionmentioning

confidence: 99%

<p>CircRNA ZNF609 Knockdown Suppresses Cell Growth via Modulating miR-188/ELF2 Axis in Nasopharyngeal Carcinoma</p>

2020

OTT

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Background: Circular RNAs (circRNAs) and microRNAs (miRNAs) have been reported to act as the important regulators in nasopharyngeal carcinoma (NPC). CircRNA ZNF609 (circ-ANF609) and miR-188 have been, respectively, reported to play a pro-cancer and anti-cancer role in NPC. The purpose of this study is to reveal the functional relation of circ-ZNF609 and miR-188 in NPC development. Methods: The transcription level and protein level of genes were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay, respectively. Cell proliferation was analyzed using 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Furthermore, flow cytometry analysis was used to assess cell cycle transition and cell apoptosis rate. Besides, the interaction between miR-188 and circ-ZNF609 or E74-like factor 2 (ELF2) was predicted by starbase or microT-CDS, and then confirmed by the dual luciferase reporter assay and RIP assay. Results: Circ-ZNF609 and ELF2 levels were increased and miR-188 level was decreased in NPC. Circ-ZNF609 knockdown significantly inhibited cell proliferation and cell cycle transition, as well as accelerated apoptosis in NPC cells. Interestingly, circ-ZNF609 directly bound to miR-188. Circ-ZNF609 regulated NPC cell growth through modulating miR-188 expression. In addition, miR-188 suppressed NPC cell growth via directly targeting ELF2. Finally, we confirmed that circ-ZNF609 mediated miR-188 level to modulate ELF2 expression. Conclusion: Our findings demonstrated that circ-ZNF609 depletion-repressed proliferation and cell cycle transition, and induced apoptosis of NPC cells via modulation of miR-188/ ELF2 axis, providing potential targets for the therapy of NPC.

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miR-188 Inhibits Glioma Cell Proliferation and Cell Cycle Progression Through Targeting β-Catenin

Cited by 25 publications

References 8 publications

LncRNA CASC11 promotes cancer cell proliferation in hepatocellular carcinoma by inhibiting miRNA-188-5p

LncRNA CASC11 promotes cancer cell proliferation in hepatocellular carcinoma by inhibiting miRNA-188-5p

MicroRNAs as Potential Biomarkers in Merkel Cell Carcinoma

<p>CircRNA ZNF609 Knockdown Suppresses Cell Growth via Modulating miR-188/ELF2 Axis in Nasopharyngeal Carcinoma</p>

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