Literature DB >> 28121348

miR-542-3p targets sphingosine-1-phosphate receptor 1 and regulates cell proliferation and invasion of breast cancer cells.

H-X Wu1, G-M Wang, X Lu, L Zhang.   

Abstract

OBJECTIVE: MicroRNAs (miRs) regulate the proliferation and metastasis of numerous cancer cell types. This study aimed to reveal the role of microRNA-542-3p (miR-542-3p) in breast cancer (BC) cell proliferation and its potential mechanisms.
MATERIALS AND METHODS: MiR-542-3p expression was detected by reverse transcription-polymerase chain reaction (RT-PCR) and sphingosine-1-phosphate receptor 1(S1PR1) protein expression was measured by Western blotting. TargetScan was used to predict the downstream target genes of miR-542-3p, which were confirmed by luciferase and RNA immunoprecipitation assays. Biological functions of miR-542-3p and S1PR1 were analyzed using CKK-8, colony formation, migration, and invasion.
RESULTS: It was demonstrated that the expression of miR-542-3p was downregulated in BC tissues and cell lines. We also showed that the expression of S1PR1 was upregulated in BC tissues and cell lines. Furthermore, we found that the expression level of miR-542-3p was negatively correlated with the expression level of S1PR1 in BC tissues. Over-expression of miR-542-3p inhibited BC cell proliferation, colony formation, migration and invasion. The dual luciferase reporter experiments showed that miR-542-3p regulated the expression of S1PR1 by combining with its 3'UTR. Finally, we showed that down-expression of miR-542-3p inhibited BC cell proliferation, colony formation, migration and invasion.
CONCLUSIONS: Our study provides the new insight that miR-542-3p inhibited colon cancer cells via targeting S1PR1, suggesting that miR-542-3p/S1PR1 can serve as a potential therapeutic target for BC.

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Year:  2017        PMID: 28121348

Source DB:  PubMed          Journal:  Eur Rev Med Pharmacol Sci        ISSN: 1128-3602            Impact factor:   3.507


  12 in total

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10.  Hsa-miR-5581-3p and Hsa-miR-542-3p Target the F8 Gene in Hemophilia A without F8 Mutations.

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