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MiR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.

ABSTRACT: Increasing evidence suggests that long non coding (lnc)RNA and microRNA (miRNA/miR) both regulate the expression of key genes in tumorigenesis and have considerable theranostic potential. Rapid advances in bioinformatics indicate that miRNA may potentially interact with lncRNA to modulate their regulatory roles. miR-148b-3p has been reported to have a vital role in regulating tumor progression. However, the expression pattern of miR-148b-3p in glioma remains largely unknown, and interactions between miR-148b-3p and lncRNA has yet to be identified. The aim of the present study was to insight into the regulatory role of miR-148b-3p in glioma. Using online software, the HOTAIR gene was identified as a possible lncRNA target of miR-148b-3p in the present study. siRNA was used to suppress the expression of HOTAIR and reverse transcription-quantitative polymerase chain reaction was used to detect the expression of miR-148b-3p. The results confirmed that HOTAIR mRNA expression was inversely correlated with miR-148b-3p expression in A172 glioma cells. Furthermore, a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was performed to detect the viability of cells, flow cytometry was performed to test cell cycle and a matrigel invasion assay was performed to test cell invasion. The results showed that HOTAIR promotes factors associated with malignancy, including cell proliferation, cell cycle progression and invasion, whereas miR-148b-3p suppresses malignancy. Bioinformatics and luciferase reporter assays showed that miR-148b-3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence. In summary, the results indicated that miR-148b-3p inhibits malignant biological behaviors of glioma cells by directly targeting HOTAIR. The current data provide important evidence for understanding the key roles of the lncRNA miRNA functional network in glioma.

SUBMITTER: Wang G

PROVIDER: S-EPMC4950229 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature

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miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high <i>HOTAIR</i> expression.

Wang Guan G Li Zhaohui Z Tian Nan N Han Liang L Fu Yao Y Guo Zhigang Z Tian Yu Y

Oncology letters 20160616 2

Increasing evidence suggests that long non coding (lnc)RNA and microRNA (miRNA/miR) both regulate the expression of key genes in tumorigenesis and have considerable theranostic potential. Rapid advances in bioinformatics indicate that miRNA may potentially interact with lncRNA to modulate their regulatory roles. miR-148b-3p has been reported to have a vital role in regulating tumor progression. However, the expression pattern of miR-148b-3p in glioma remains largely unknown, and interactions bet ...[more]

PMID: 27446363

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Project description:BackgroundGlioma is the most common and lethal type of malignant brain tumor. Accumulating evidence has highlighted that RNA binding protein APOBEC1 complementation factor (A1CF) is involved in various cellular processes by modulating RNA expression, and acts as an oncogene in breast cancer. However, the function of A1CF in glioma remained unclear.MethodsQuantitative RT-PCR and western blot analysis were employed to detect the expression levels of A1CF, lncRNA family with sequence similarity 224 member A (FAM224A), miR-590-3p, zinc finger protein 143 (ZNF143) and ArfGAP with SH3 domain, ankyrin repeat and PH domain 3 (ASAP3) in glioma tissues and cell lines. The Cell Counting Kit-8 assay, migration and invasion assays, and flow cytometry analysis were conducted to evaluate the function of A1CF, FAM224A, miR-590-3p, ZNF143 and ASAP3 in the malignant biological behaviors of glioma cells. Moreover, luciferase reporter, RIP and ChIP assays were used to investigate the interactions among A1CF, FAM224A, miR-590-3p, ZNF143, ASAP3 and MYB. Finally, the xenograft tumor growth assay further ascertained the biological roles of A1CF, FAM224A and miR-590-3p in glioma cells.ResultsA1CF was upregulated and functioned as an oncogene via stabilizing and increasing FAM224A expression; moreover, high A1CF and FAM224A expression levels indicated a poorer prognosis for glioma patients. Conversely, miR-590-3p was downregulated and exerted a tumor-suppressive function in glioma cells. Inhibition of A1CF significantly restrained cell proliferation, migration and invasion, and promoted apoptosis by upregulating miR-590-3p in a FAM224A-dependent manner. FAM224A was a molecular sponge of miR-590-3p and they were in an RNA-induced silencing complex. ZNF143 was upregulated in glioma tissues and cell lines. MiR-590-3p could negatively modulate the expression of ZNF143 via binding to the ZNF143 3' UTR. Moreover, ZNF143 participated in miR-590-3p-induced tumor-suppressive activity on glioma cells. ASAP3 and MYB were transcriptionally activated by ZNF143, and importantly, ZNF143 could directly target the promoter of FAM224A and stimulate its expression, collectively forming a positive feedback loop.ConclusionsThe present study clarifies that the A1CF-FAM224A-miR-590-3p-ZNF143 positive feedback loop conducts critical regulatory effects on the malignant progression of glioma cells, which provides a novel molecular target for glioma therapy.

Dataset Information

MiR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.

Publications

miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high <i>HOTAIR</i> expression.

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