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MiR-601 inhibits proliferation, migration and invasion of prostate cancer stem cells by targeting KRT5 to inactivate the Wnt signaling pathway.

ABSTRACT: OBJECTIVE:This study aimed to verify the hypothesis that downregulation of miR-601 inhibits the proliferation, migration, and invasion of prostate cancer stem cells (PCSCs) by the Wnt signaling pathway through targeting keratin 5 (KRT5). METHODS:Bioinformatic tools were applied to predict miRNAs and genes potentially associated with prostate cancer, then miR-601 and KRT5 were selected. Subsequently, PCSCs were investigated with respect to miR-601 overexpression or inhibition, KRT5 overexpression, or treatment with a Wnt pathway inhibitor. A series of experiments including western blotting, RT-qPCR, wound healing experiment, transwell assay, MTT assay, annexin V-FITC/PI flow cytometric analysis, nude mice assay and immunohistochemistry were then carried out. RESULTS:Compared with negative control group, migration, invasion, and proliferation of PCSCs and Wnt-1 expression were all enhanced, but apoptosis was attenuated in the miR-601 mimic group. Furthermore, results identified in the other groups (KRT5, miR-601 inhibitor, miR-601 inhibitor + KRT5, Wnt signaling pathway inhibitor, PRI-724/PRI-724 + KRT5) were opposite to those identified with the miR-601 mimic group (all P<0.05). Compared with the miR-601 inhibitor + KRT5 group, migration, invasion, and proliferation of PCSCs and Wnt-1 expression were all increased, whereas apoptosis was suppressed in KRT5 or miR-601 inhibitor groups (all P<0.05). Compared with the PRI-724 + KRT5 group, migration, invasion, and proliferation of PCSCs and Wnt-1 expression were also enhanced, whereas apoptosis was inhibited in PRI-724 or KRT5 groups (all P<0.05). CONCLUSION:Results obtained from the present study have demonstrated that downregulation of miR-601 is able to inhibit the proliferation, migration, and invasion of PCSCs by activating KRT5, and subsequently inhibiting the Wnt pathway.

SUBMITTER: Du H

PROVIDER: S-EPMC6949885 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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miR-601 inhibits proliferation, migration and invasion of prostate cancer stem cells by targeting KRT5 to inactivate the Wnt signaling pathway.

Du Hongbing H Wang Xinghuan X Dong Rui R Hu Dongliang D Xiong Yaoyi Y

International journal of clinical and experimental pathology 20191201 12

<h4>Objective</h4>This study aimed to verify the hypothesis that downregulation of miR-601 inhibits the proliferation, migration, and invasion of prostate cancer stem cells (PCSCs) by the Wnt signaling pathway through targeting keratin 5 (KRT5).<h4>Methods</h4>Bioinformatic tools were applied to predict miRNAs and genes potentially associated with prostate cancer, then miR-601 and KRT5 were selected. Subsequently, PCSCs were investigated with respect to miR-601 overexpression or inhibition, KRT5 ...[more]

PMID: 31933840

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Project description:BackgroundG protein-coupled bile acid receptor 1 (GPBAR1) is a G protein-coupled receptor for bile acids, which is widely expressed in many human tissues. Patchouli alcohol (PA) has been shown to have an anti-cancer effect, including in prostate cancer (PCa). This study sought to confirm the regulatory mechanism of GPBAR1 in the anti-cancer activity of PA in PCa.MethodsThe SwissTargetPrediction website (Pro >0) was used to predict the target of PA. The UALCAN and The Cancer Genome Atlas-Prostate cohort was used to examine the differentially expressed genes and PCa recurrence. A gene set enrichment analysis (GSEA) was conducted to analyze the relationship between the expression of GPBAR1 and PCa proliferation, migration, and invasion. Cell proliferation, migration, and invasion were assessed by colony formation, 5-Ethynyl-2'-deoxyuridine staining, cell scratch assays, and Transwell invasion assays, respectively. A xenograft animal model was established to assess the effect of PA on tumor growth in vivo. GPBAR1 protein and apoptosis related protein expression was measured by western blot.ResultsGPBAR1 was a PA target predicted by the SwissTargetPrediction website. PA inhibited the expression of GPBAR1 in PCa cells in a time- and dose-dependent manner. The abnormal expression of GPBAR1 was related to cell proliferation, migration, and invasion. Additionally, GPBAR1 overexpression promoted the cell proliferation, migration, and invasion, and inhibited the apoptosis of PCa cells. GPBAR1 silencing inhibited the cell proliferation, migration, and invasion, and promoted the apoptosis of PCa cells. High expressions of GPBAR1 suppressed tumor growth in tumor-bearing mice. Further, GPBAR1 promoted the activation of nuclear factor kappa B (NF-κB) signaling, and PA regulated the malignant phenotypes of PCa cells via the NF-κB signaling pathway mediated by GPBAR1.ConclusionsGPBAR1 is a promising drug target of PA, and was shown to regulate the proliferation, apoptosis, migration, and invasion of PCa cells through GPBAR1/NF-κB inhibition.

Dataset Information

MiR-601 inhibits proliferation, migration and invasion of prostate cancer stem cells by targeting KRT5 to inactivate the Wnt signaling pathway.

Publications

miR-601 inhibits proliferation, migration and invasion of prostate cancer stem cells by targeting KRT5 to inactivate the Wnt signaling pathway.

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