Dataset Information

MIR-138-5P inhibits the progression of prostate cancer by targeting FOXC1.

ABSTRACT: BACKGROUND:Studies have suggested that micro-RNAs (miRNAs) can function as an oncogene or a tumor suppressor in cancers. However, the role of MIR-138-5P (613394) in prostate cancer (PCa) remains unclear. METHODS:Expression level of MIR-138-5P in PCa cell lines and normal cell line was analyzed with the quantitative real-time PCR method. Cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were performed to analyze the biological functions of MIR-138-5P. RESULTS:We showed MIR-138-5P expression level was significantly decreased in PCa cell lines compared with the normal cell line. Overexpression of MIR-138-5P inhibits PCa cell proliferation, colony formation, cell migration, and cell invasion in vitro. Mechanistically, we showed Forkhead box C1 (FOXC1, 601090) was a direct target for MIR-138-5P in PCa. We confirmed that overexpression of FOXC1 partially reversed the effects of MIR-138-5P on PCa cell behaviors. CONCLUSIONS:Collectively, we showed that MIR-138-5P functions as a tumor suppressor gene in PCa via targeting FOXC1.

SUBMITTER: Huang H

PROVIDER: S-EPMC7196466 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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MIR-138-5P inhibits the progression of prostate cancer by targeting FOXC1.

Huang Hui H Xiong Ying Y Wu Zhensheng Z He Yuhui Y Gao Xianglin X Zhou Zhangyan Z Wang Tao T

Molecular genetics & genomic medicine 20200228 4

<h4>Background</h4>Studies have suggested that micro-RNAs (miRNAs) can function as an oncogene or a tumor suppressor in cancers. However, the role of MIR-138-5P (613394) in prostate cancer (PCa) remains unclear.<h4>Methods</h4>Expression level of MIR-138-5P in PCa cell lines and normal cell line was analyzed with the quantitative real-time PCR method. Cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were performed to analyze the biological func ...[more]

PMID: 32107877

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Project description:BACKGROUND:Non small cell lung cancer (NSCLC) is one of the most common cancers in the world. DHA is known to be capable of suppressing NSCLC cell proliferation and metastasis. However, the mechanisms by which DHA exhibits its antitumor effects are unknown. Here we aimed to identify the effects and mechanisms of DHA and its metabolites on lung cancer cell growth and invasion. METHODS:As measures of cell proliferation and invasion ability, the cell viability and transwell assays were used in vitro. Transgenic mfat-1 mice, which convert ω-6 PUFAs to ω-3 PUFAs, were used to detect the effect of endogenous DHA on tumor transplantation. An LC - MS/MS analysis identified the elevation of several eicosanoid metabolites of DHA. By using qPCR miRNA microarray, online prediction software, luciferase reporter assays and Western blot analysis, we further elucidated the mechanisms. RESULTS:Addition of exogenous DHA inhibited the growth and invasion in NSCLC cells in vitro. Endogenously produced DHA attenuated LLC-derived tumor growth and metastasis in the transgenic mfat-1 mice. Among the elevation of DHA metabolites, resolvin D1 (RvD1) significantly contributed to the inhibition in cell growth and invasion. MiRNA microarray revealed that the level of miR-138-5p was significantly increased after RvD1 treatment. MiR-138-5p mimics decreased cell viability and invasion; while miR-138-5p inhibitor abolished RvD1-mediated suppression of cell viability and invasion. The expression of FOXC1 was significantly reduced upon overexpression of miR-138-5p while luciferase reporter assay showed that FOXC1 was a direct target of miR-138-5p. In vivo, endogenous DHA by the mfat-1 transgene enhanced miR-138-5p expression and decreased FOXC1 expression. Furthermore, overexpression of FOXC1 reversed the inhibition in cell viability and invasion induced by RvD1 treatment. CONCLUSIONS:These data identified the RvD1/miR-138-5p/FOXC1 pathway as a novel mechanism by DHA and its metabolite, RvD1, and the potential of targeting such pathway as a therapeutic strategy in treating NSCLC.

Dataset Information

MIR-138-5P inhibits the progression of prostate cancer by targeting FOXC1.

Publications

MIR-138-5P inhibits the progression of prostate cancer by targeting FOXC1.

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