MiR-524-5p Suppresses Migration, Invasion, and EMT Progression in Breast Cancer Cells Through Targeting<i>FSTL1</i>

Jin, Taobo; Zhang, Yun; Zhang, Tianya

doi:10.1089/cbr.2019.3046

Cited by 19 publications

(17 citation statements)

References 41 publications

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“…microRNAs are also crucial players involved in tumorigenesis 23 . For example, both miR‐197‐3p and miR‐451a are down‐regulated in PCa, and they inhibit the proliferation and invasion of PCa cells, and promote their apoptosis 24,25 .…”

Section: Discussionmentioning

confidence: 99%

“…microRNAs are also crucial players involved in tumorigenesis. 23 For example, both miR-197-3p and miR-451a are down-regulated in PCa, and they inhibit the proliferation and invasion of PCa cells, and promote their apoptosis. 24,25 miR-384 is a tumor suppressor, which is down-regulated in osteosarcoma and papillary thyroid cancer, and inhibits tumor growth.…”

Section: Discussionmentioning

confidence: 99%

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Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Shi

Zhang

Song

et al. 2021

The Journal of Gene Medicine

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Background Multiple long non‐coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression. Methods A quantitative real‐time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA‐384 (miR‐384) and homeobox B7 (HOXB7) expression. Call‐couting kit‐8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual‐luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR‐384, SNHG8 and HOXB7. Results SNHG8 was up‐regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR‐384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR‐384 inhibition. HOXB7 was confirmed to be a target gene of miR‐384. SNHG8 knockdown repressed HOXB7 expression via targeting miR‐384. Conclusions SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR‐384 and up‐regulating HOXB7.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Shi

Zhang

Song

et al. 2021

The Journal of Gene Medicine

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“…Among miR-200c predicted targets, we found FSTL1. Since it has been recently documented the importance of epicardial FSTL1 in cardiac regeneration [ 21 ] and its involvement in airway and cancer EMT [ 28 , 29 ], we hypothesized that (1) FSTL1 could be also involved in epicardial EMT (2) through a miR-200c-dependent pathway.…”

Section: Resultsmentioning

confidence: 99%

“…Further, previous results already demonstrated that FSTL1 induced EMT in the airways of patients and mice by activating autophagy, and miR-524-5p/FSTL1 has the ability of regulating the progression of EMT of breast cancer cells [ 28 , 29 ]. Similarly, in our study, using an in vivo model of myocardial infarction in mice, we detected a strong upregulation of FSTL1 in epicardial cells undergoing EMT during acute MI.…”

Section: Discussionmentioning

confidence: 99%

miR-200c-3p Regulates Epitelial-to-Mesenchymal Transition in Epicardial Mesothelial Cells by Targeting Epicardial Follistatin-Related Protein 1

Pontemezzo

Foglio

Vernucci

et al. 2021

IJMS

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Recent findings suggest that epithelial to mesenchymal transition (EMT), a key step during heart development, is involved in cardiac tissue repair following myocardial infarction (MI). MicroRNAs (miRNAs) act as key regulators in EMT processes; however, the mechanisms by which miRNAs target epicardial EMT remain largely unknown. Here, by using an in vitro model of epicardial EMT, we investigated the role of miRNAs as regulators of this process and their potential targets. EMT was induced in murine epicardial-mesothelial cells (EMCs) through TGF β1 treatment for 48, 72, and 96 h as indicated by the expression of EMT-related genes by qRT-PCR, WB, and immunofluorescence. Further, enhanced expression of stemness genes was also detected. Among several EMT-related miRNAs, miR-200c-3p expression resulted as the most strongly suppressed. Interestingly, we also found a significant upregulation of Follistatin-related protein 1 (FSTL1), a miR-200c predicted target already identified as a potent cardiogenic factor produced by epicardial cells that promotes regeneration following MI. Dual-luciferase reporter assay demonstrated that miR-200c-3p directly targeted the 3′-untranslated region of FSTL1 in EMCs. Consistently, WB analysis showed that knockdown of miR-200c-3p significantly increased FSTL1 expression, whereas overexpression of miR-200c-3p counteracted TGF β1-mediated FSTL1 upregulation. Importantly, FSTL1 silencing maintained epithelial features in EMCs, despite EMT induction by TGF β1, and attenuated EMT-associated traits, including migration and stemness. In conclusion, epicardial FSTL1, an important cardiogenic factor in its secreted form, induces EMT, stemness, and migration of EMCs in a miR-200c-3p dependent pathway.

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“…Our results suggest that LINC00313 upregulates the expression of the pro-apoptotic proteins Bax and caspase-3/9 and inhibits the expression of the anti-apoptotic protein Bcl-2. E-cadherin, N-cadherin, Vimentin, and MMP-2 are markers of cell migration and invasion [29]. N-cadherin, Vimentin, and MMP-2 expression was signi cantly inhibited in response to the overexpression of LINC00313 in cells, and E-cadherin expression was signi cantly increased in response to LINC00313 overexpression.…”

Section: Discussionmentioning

confidence: 99%

WGCNA Co-Expression Network Analysis Reveals LncRNA LINC00313 Functions as A ceRNA to Regulate PTEN-Mediated PI3K/AKT Signaling Pathway by Sponging miR-19a-3p in Docetaxel-Resistant Prostate Cancer Cells

Chen

Zhang

et al. 2020

Preprint

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Background: Docetaxel is the preferred chemotherapeutic agent for patients with hormone-refractory PCa. LncRNAs play important roles in the development of docetaxel resistance in patients with PCa. We evaluated the effects of the lncRNA LINC00313 on growth and metastasis in docetaxel-resistant PCa cells, and the molecular mechanisms underlying these effects.Methods: The mRNA dataset (GSE102124 and GSE55945) and lncRNA dataset (GSE115414) were downloaded from the GEO database. The DEGs were identified using the “R package limma”. WGCNA were performed to identify the modules and genes associated with PCa. A PPI network was constructed using the STRING database and visualized using Cytoscape. The Cytohubba plug-in was used to identify the hub genes and cytoNCA plug-in was used to identify the highest linkage hub genes. Based on lncRNA-miRNA pairs and miRNA-mRNA pairs using StarBase and TargetScan databases, a ceRNA network was constructed. Functional analysis was performed via GO, GSEA, and GSVA analysis. Cell proliferation, apoptosis, cell cycle progression, migration, and invasion were evaluated by CCK-8, colony formation, flow cytometry, transwell, and wound healing assays. RT-PCR, western blot, and immunohistochemistry were used to evaluate mRNA and protein expression. The oncogenicity of LINC00313 in docetaxel-resistant PCa cells was determined by tumor transplantation in nude mice. Luciferase reporter and RNA pull-down assays were used to evaluate interactions between LINC00313 and miR-19a-3p as well as between miR-19a-3p and PTEN.Results: LINC00313-miR-19a-3p-PTEN was a core network of ceRNA network. Cox regression analysis identified LINC00313 as an independent prognostic variable for OS in patients with PCa. LINC00313 overexpression in docetaxel-resistant PCa cells suppressed proliferation, invasion, and migration, and induced apoptosis and cell cycle arrested at the G1 phase. These changes were related to changes in cyclinD1, p27, Ki67, Bax, Bcl-2, caspase-3/9, E-cadherin, N-cadherin, Vimentin, and MMP-2 expression. Animal experiments showed that LINC00313 silencing promoted tumor formation. Co-transfection with LINC00313‐WT and miR-19a-3p mimic reduced luciferase activity, and co-transfection with PTEN‐WT and LINC00313 increased luciferase activity. The effects of LINC00313, including increased PTEN, decreased PIP3 expression, and the inhibition of proliferation and metastasis in docetaxel-resistant PC cells, were abolished by miR-19a-3p mimic.Conclusion: LINC00313 overexpression suppressed the proliferation and metastasis of docetaxel-resistant PC cells by competitively binding to miR-19a-3p to regulate PTEN expression and inhibit the activation of the PI3K/Akt signaling pathway.

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MiR-524-5p Suppresses Migration, Invasion, and EMT Progression in Breast Cancer Cells Through TargetingFSTL1

Cited by 19 publications

References 41 publications

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

miR-200c-3p Regulates Epitelial-to-Mesenchymal Transition in Epicardial Mesothelial Cells by Targeting Epicardial Follistatin-Related Protein 1

WGCNA Co-Expression Network Analysis Reveals LncRNA LINC00313 Functions as A ceRNA to Regulate PTEN-Mediated PI3K/AKT Signaling Pathway by Sponging miR-19a-3p in Docetaxel-Resistant Prostate Cancer Cells

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