miR-150-5p mediates extravillous trophoblast cell migration and angiogenesis functions by regulating VEGF and MMP9

Zeng, Yu; Wei, Lijie; Lali, Mwamaka Sharifu; Chen, Yuting; Yu, Jun; Li, Feng

doi:10.1016/j.placenta.2020.02.019

Cited by 31 publications

(22 citation statements)

References 38 publications

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“…Our mechanistic research further revealed that miR-519d targeted LEP. Burgeoning investigation has confirmed that miRNAs can exert various effects on PE progression [ 29 , 30 , 31 ]. Similar to our present results, prior work also showed aberrant downregulated expression of miR-519d in PE [ 14 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

miR-519d downregulates LEP expression to inhibit preeclampsia development

Cai

et al. 2021

Open Medicine

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The purpose of the current study was to characterize role of microRNA (miR)-519d in trophoblast cells and preeclampsia (PE) development and its potential underlying mechanism. Regulation of leptin (LEP) by miR-519d was verified using a dual-luciferase reporter gene assay. Loss- and gain-of-function assays were conducted to detect the roles of miR-519d and LEP in proliferation, migratory ability, and invasive capacity of HTR-8/SVneo cells by means of CCK-8 assay, scratch test, and Transwell invasion assay, respectively. The cell apoptosis rate and cycle distribution were analyzed by flow cytometry. LEP expression was elevated, whereas miR-519d level was suppressed in the PE placenta samples compared with those from normal pregnancy. Depletion of LEP promoted proliferation, migratory ability, and invasive capacity and repressed apoptosis. miR-519d could bind 3′ untranslated regions (3′UTRs) of LEP, the extent of which correlated negatively with LEP expression. miR-519d suppressed the expression of LEP in HTR-8/SVneo cells. Moreover, overexpression of miR-519d promoted survival and migratory ability of HTR-8/SVneo cells. Taken together, we find that miR-519d targeted LEP and downregulated its expression, which could likely inhibit the development of PE.

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Section: Discussionmentioning

confidence: 99%

miR-519d downregulates LEP expression to inhibit preeclampsia development

Cai

et al. 2021

Open Medicine

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“…Another finding of present study was that administration of bacteria with cardiac peptides expressing constructs could reduce MMP-9 expression under hypoxic condition in vivo. Different studies have now suggested a key role for MMP9 in development of a proper microenvironment for promotion of tumor growth and angiogenesis by enhancing the interrelation between VEGF and VEGFR2 [ 45 , 46 ]. This mainly takes place through the proteolytic cleavage and release of extracellular matrix (ECM) bound VEGF by MMP9 activity which is an important step in angiogenic switch.…”

Section: Discussionmentioning

confidence: 99%

Engineered hypoxia-responding Escherichia coli carrying cardiac peptide genes, suppresses tumor growth, angiogenesis and metastasis in vivo

et al. 2021

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Development of engineered non-pathogenic bacteria, capable of expressing anti-cancer proteins under tumor-specific conditions, is an ideal approach for selectively eradicating proliferating cancer cells. Herein, using an engineered hypoxia responding nirB promoter, we developed an engineered Escherichia coli BW25133 strain capable of expressing cardiac peptides and GFP signaling protein under hypoxic condition for spatiotemporal targeting of mice mammary tumors. Following determination of the in vitro cytotoxicity profile of the engineered bacteria, selective accumulation of bacteria in tumor microenvironment was studied 48 h after tail vein injection of 108 cfu bacteria in animals. For in vivo evaluation of antitumoral activities, mice with establishment mammary tumors received 3 consecutive intravenous injections of transformed bacteria with 4-day intervals and alterations in expression of tumor growth, invasion and angiogenesis specific biomarkers (Ki-67, VEGFR, CD31and MMP9 respectively), as well as fold changes in concentration of proinflammatory cytokines were examined at the end of the 24-day study period. Intravenously injected bacteria could selectively accumulate in tumor site and temporally express GFP and cardiac peptides in response to hypoxia, enhancing survival rate of tumor bearing mice, suppressing tumor growth rate and expression of MMP-9, VEGFR2, CD31 and Ki67 biomarkers. Applied engineered bacteria could also significantly reduce concentrations of IL-1β, IL-6, GC-SF, IL-12 and TNF-α proinflammatory cytokines while increasing those of IL-10, IL-17A and INF-γ. Overall, administration of hypoxia-responding E. coli bacteria, carrying cardiac peptide expression construct could effectively suppress tumor growth, angiogenesis, invasion and metastasis and enhance overall survival of mice bearing mammary tumors.

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“…MALAT1 regulation of miR-150-5p is also reported in various conditions (18)(19)(20)(21)(22). miR-150-5p regulation of VEGFA is also reported in various conditions (23)(24)(25)(26). Hence, we investigated whether MALAT1 regulation of miR-150-5p/ VEGFA signaling plays a role in OS-induced angiogenesis.…”

Section: Lncrna Malat1 Expression In Os Suppress Proliferation and Migration Of Endothelial Cellsmentioning

confidence: 87%

“…LncRNA TNK2-AS1 regulated oxidized low-density lipoprotein-stimulated human aortic smooth muscle cell proliferation and migration by VEGFA/miR-150-5p axis (25). miR-150-5p/VEGFA signaling mediates extravillous trophoblast cell migration and angiogenesis (26). Hence, we speculate that MALAT1 may play a role in the control of miR-150-5p, instructing OS to release VEGFA in their microenvironment in order to induce angiogenesis.…”

Section: Lncrna Malat1 Expression In Os Suppress Proliferation and Migration Of Endothelial Cellsmentioning

confidence: 90%

LncRNA MALAT1 Promotes Tumor Angiogenesis by Regulating MicroRNA-150-5p/VEGFA Signaling in Osteosarcoma: In-Vitro and In-Vivo Analyses

2021

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The present study aims to analyze the expression of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in human osteosarcoma (OS) cells and to investigate its role in OS-induced angiogenesis. MALAT1 expression in OS cells was significantly higher than in normal osteoblasts. The functional analysis indicated that MALAT1 appears to enhance OS-induced angiogenesis, in vitro and in vivo analyses, endothelial cell proliferation and migration, chick embryo angiogenesis assay, and zebrafish xenograft model. Mechanistically, silencing MALAT1 downregulated vascular endothelial growth factor A (VEGFA) expression and upregulated miR-150-5p expression in OS cells, and MALAT1-mediated angiogenic induction by VEGFA in OS microenvironment. Moreover, MALAT1 directly targeted miR-150-5p and miR-150-5p directly target VEGFA in OS. Overexpression of miR-150-5p downregulates VEGFA expression in OS. More notably, we showed that MALAT1 induced angiogenesis in OS microenvironment by upregulating the expression of VEGFA via targeting miR-150-5p. Overall, our findings suggest that MALAT1 promotes angiogenesis by regulating the miR-150-5p/VEGFA signaling in OS microenvironment. The findings of the molecular mechanisms of MALAT1 in tumor angiogenesis offer a new viewpoint on OS treatment.

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miR-150-5p mediates extravillous trophoblast cell migration and angiogenesis functions by regulating VEGF and MMP9

Cited by 31 publications

References 38 publications

miR-519d downregulates LEP expression to inhibit preeclampsia development

miR-519d downregulates LEP expression to inhibit preeclampsia development

Engineered hypoxia-responding Escherichia coli carrying cardiac peptide genes, suppresses tumor growth, angiogenesis and metastasis in vivo

LncRNA MALAT1 Promotes Tumor Angiogenesis by Regulating MicroRNA-150-5p/VEGFA Signaling in Osteosarcoma: In-Vitro and In-Vivo Analyses

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