scholarly journals miR-373-3p Regulates Invasion and Migration Abilities of Trophoblast Cells via Targeted CD44 and Radixin

2021 ◽  
Vol 22 (12) ◽  
pp. 6260
Author(s):  
Hyun-Jung Lee ◽  
Seung Mook Lim ◽  
Hee Yeon Jang ◽  
Young Ran Kim ◽  
Joon-Seok Hong ◽  
...  
Keyword(s):  
Preterm Labor ◽  
Target Genes ◽  
Gene Array ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Invasion And Migration ◽  
Mirna Array ◽  
Qrt Pcr ◽  
Putative Target ◽  
And Migration

Preterm labor (PTL) is one of the obstetric complications, and is known to be associated with abnormal maternal inflammatory response and intrauterine inflammation and/or infection. However, the expression of specific miRNAs associated with PTL is not clear. In this study, we performed combination analysis of miRNA array and gene array, and then selected one miRNA (miR-373-3p) and its putative target genes (CD44 and RDX) that exhibited large expression differences in term and PTL placentas with or without inflammation. Using qRT-PCR and luciferase assays, we confirmed that miR-373-3p directly targeted CD44 and RDX. Overexpression of miR-373-3p reduced the migration and invasion of trophoblast cells, while inhibition of miR-373-3p restored the migration and invasion abilities of trophoblast cells. Finally, we validated the expression of miR-373-3p and its target genes in clinical patients’ blood. miR-373-3p was increased in PTL patients’ blood, and was the most expressed in PTL patients’ blood with inflammation. In addition, by targeting the miR-373-3p, CD44 and RDX was decreased in PTL patients’ blood, and their expression were the lowest in PTL patients’ blood with inflammation. Taken together, these findings suggest that miR-373-3p and its target genes can be potential biomarkers for diagnosis of PTL.

scholarly journals miR-17-5p promotes the invasion and migration of colorectal cancer by regulating HSPB2

2020 ◽  
Author(s):  
Wei fang Yu ◽  
Jia Wang ◽  
Chao Li ◽  
Mingda Xuan ◽  
Shuangshuang Han ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Lymph Node ◽  
Target Genes ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Node Metastasis ◽  
Rescue Experiment ◽  
And Migration

Abstract Background: MicroRNA (miRNA) can affect tumor progression by regulating cell proliferation, apoptosis and metastasis. After miRNA microarray chip analysis of colorectal cancer (CRC) tissues and adjacent normal tissues, a significant upregulation of miR-17-5p expression was found in CRC tissues. However, the underlying mechanism of miR-17-5p in CRC is still unclear.Methods: The levels of miR-17-5p in 47 paired CRC and adjacent normal tissue samples were determined by quantitative real-time PCR (qRT-PCR). CCK-8, colony formation, flow cytometry and transwell assays were used to explore the biological effects of miR-17-5p on CRC cells. In addition, the transcriptome sequencing and miRNA target prediction software were employed to identify targets of miR-17-5p. Luciferase reporter detection was used to demonstrate the direct binding of target genes by miR-17-5p. The rescue experiment was conducted to investigate the biological function of target genes and regulatory mechanism of miR-17-5p on target genes.Results: The expression of miR-17-5p was significantly higher in CRC tissues than in adjacent normal tissues. In CRC group, the expression of miR-17-5p in cancer tissues with lymph node metastasis was higher compared with those without lymph node metastasis. Overexpression of miR-17-5p inhibited CRC cell apoptosis, as well as promoting proliferation, migration and invasion. We hypothesized that HSPB2 might be a target gene of miR-17-5p and validated for the first time that miR-17-5p binds directly to the 3’-UTR of HSPB2. In the rescue experiment, the tumor suppressive effect of HSPB2 was detected and miR-17-5p could promote cell proliferation, migration and invasion by targeting HSPB2.Conclusion: MiR-17-5p promotes invasion and migration by inhibiting HSPB2 in CRC, thereby implicating its potential as a novel diagnostic biomarker and therapeutic target for CRC.

scholarly journals miR-183-5p suppressed the invasion and migration of HTR-8/SVneo trophoblast cells partly via targeting MMP-9 in preeclampsia

2020 ◽  
Vol 40 (6) ◽  
Author(s):  
Mingli Suo ◽  
Yanfei Sun ◽  
Hailan Yang ◽  
Jing Ji ◽  
Yinfang He ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Cell Invasion ◽  
Underlying Mechanism ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Down Regulation ◽  
Invasion And Migration ◽  
Potential Biomarker ◽  
And Migration

Abstract Preeclampsia (PE), a common obstetrical disorder, is characterized by impaired migration and invasion abilities of trophoblastic cells. MicroRNA-183-5p (miR-183) was reported to regulate cell migration and invasion in various types of human cancers; however, its role in the pathogenesis of PE remains elusive. Herein, we investigated the role of miR-183 in HTR-8/SVneo trophoblast cells invasion and migration and explored the underlying mechanism. Our results showed that miR-183 was significantly up-regulated in placental tissues from pregnant women compared with that in normal pregnant women. Overexpression of miR-183 inhibited proliferation, migration and invasion, as well as induced apoptosis in HTR-8/SVneo cells. Otherwise, down-regulation of miR-183 achieved the opposite effects. Bioinformatics prediction and luciferase reporter assay confirmed that matrix metalloproteinase-9 (MMP-9) is a target of miR-183. In addition, MMP-9 expression was significantly down-regulated, and inversely correlated with the miR-183 level in placental tissues from pregnant women with severe PE. Down-regulation of MMP-9 suppressed the trophoblast cell invasion and migration, whereas overexpression of MMP-9 promoted cell invasion and migration in HTR-8/SVneo cells. More importantly, up-regulation of MMP-9 reversed the inhibitory effects of miR-183 on cell invasion and migration in trophoblast cells. Collectively, our findings suggested that miR-183 may play critical roles in the pathogenesis of PE and serve as a potential biomarker for severe PE.

scholarly journals miR-17-5p Promotes the Invasion and Migration of Colorectal Cancer by Regulating HSPB2

2020 ◽  
Author(s):  
Wei fang Yu ◽  
Jia Wang ◽  
Chao Li ◽  
Mingda Xuan ◽  
Shuangshuang Han ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Lymph Node ◽  
Target Genes ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Node Metastasis ◽  
Rescue Experiment ◽  
And Migration

Abstract Background: MicroRNA (miRNA) can affect tumor progression by regulating cell proliferation, apoptosis and metastasis. After miRNA microarray chip analysis of colorectal cancer (CRC) tissues and adjacent normal tissues, a significant upregulation of miR-17-5p expression was found in CRC tissues. However, the underlying mechanism of miR-17-5p in CRC is still unclear.Methods: The levels of miR-17-5p in 47 paired CRC and adjacent normal tissue samples were determined by quantitative real-time PCR (qRT-PCR). CCK-8, colony formation, flow cytometry and transwell assays were used to explore the biological effects of miR-17-5p on CRC cells. In addition, the transcriptome sequencing and miRNA target prediction software were employed to identify targets of miR-17-5p. Luciferase reporter detection was used to demonstrate the direct binding of target genes by miR-17-5p. The rescue experiment was conducted to investigate the biological function of target genes and regulatory mechanism of miR-17-5p on target genes.Results: The expression of miR-17-5p was significantly higher in CRC tissues than in adjacent normal tissues. In CRC group, the expression of miR-17-5p in cancer tissues with lymph node metastasis was higher compared with those without lymph node metastasis. Overexpression of miR-17-5p inhibited CRC cell apoptosis, as well as promoting proliferation, migration and invasion. We hypothesized that HSPB2 might be a target gene of miR-17-5p and validated for the first time that miR-17-5p binds directly to the 3’-UTR of HSPB2. In the rescue experiment, the tumor suppressive effect of HSPB2 was detected and miR-17-5p could promote cell proliferation, migration and invasion by targeting HSPB2.Conclusion: MiR-17-5p promotes invasion and migration by inhibiting HSPB2 in CRC, thereby implicating its potential as a novel diagnostic biomarker and therapeutic target for CRC.

scholarly journals MicroRNA-214-5p Inhibits the Invasion and Migration of Hepatocellular Carcinoma Cells by Targeting Wiskott-Aldrich Syndrome Like

2018 ◽  
Vol 46 (2) ◽  
pp. 757-764 ◽  
Author(s):  
Hongdan Li ◽  
Haoqi Wang ◽  
Zhen Ren
Keyword(s):  
Hepatocellular Carcinoma ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Hepatocellular Carcinoma Cells ◽  
Invasion And Migration ◽  
Wiskott Aldrich Syndrome ◽  
Normal Tissues ◽  
Qrt Pcr ◽  
And Migration

Background/Aims: This study aims to explore the effects of microRNA-214-5p (miR-214-5p) on the invasion and migration of Hepatocellular Carcinoma cells (HCC). Methods: Hepatocellular Carcinoma tissues and adjacent normal tissues from 44 hepatocellular carcinoma patients were prepared for this study. The HepG2 and BEL-7402 cells were transfected with miR-214-5p mimic and inhibitor. qRT-PCR was performed to detect the expressions of miR-214-5p. Transwell assays were used to detect the invasion and migration assays in HepG2 and BEL-7402 cells. A dual-luciferase reporter assay was conducted to examine the effect of miR-214-5p on Wiskott-Aldrich Syndrome Like (WASL/ N-WASP). Western blot and qRT-PCR were used to measure the expressions of the E-cadherin, N-cadherin and Vimentin proteins. Transwell chamber assays were performed to detect cell invasion and migration. Results: Compared with normal tissues, HCC tissues demonstrated significantly lower expression of miR-214-5p. Overexpression of miR-214-5p significantly inhibited the migration and invasion of HCC cells and inhibition of miR-214-5p promoted the migration and invasion. Additionally, miR-214-5p suppressed the epithelial-mesenchymal transition (EMT). Further study showed WASL was a putative target gene of miR-214-5p. Up-regulating the expression of WASL could reverse the inhibition effect of miR-214-5p on invasion and migration. Conclusion: Our data suggested that miR-214-5p inhibited the invasion and migration of HepG2 and BEL-7402 by targeting WASL in Hepatocellular carcinoma.

scholarly journals MicroRNA-490-3p inhibits migration and chemoresistance of colorectal cancer cells via targeting TNKS2

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jing Li ◽  
Rubing Mo ◽  
Linmei Zheng
Keyword(s):  
Colorectal Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Chemotherapy Resistance ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Colorectal Cancer Cells ◽  
And Migration ◽  
Common Malignancy

Abstract Objective Colorectal cancer is one of the most common malignancy in the world. The oncogenesis of colorectal cancer is still not fully elucidated. It was reported that microRNA-490-3p (miR-490-3p) was closely related to the regulation of cancers. However, if miR-490-3p could also affect colorectal cancer and the specific mechanism remains unclear. Methods qRT-PCR was conducted to examine the expression of miR-490-3p. DIANA, miRDB, and TargetScan databases were used to identify target genes. LOVO and SW480 cells were transfected by miR-490-3p mimics and inhibitors. Transwell assay was used to measure cell invasion and migration. Cisplatin and fluorouracil were administered to investigate chemotherapy resistance. Western blot was used to measure TNKS2 protein expression. Binding sites were verified using the double luciferase assay. Results miR-490-3p expression was low in the colorectal cancer cells. The level of miR-490-3p was negatively correlated with cell migration and invasion of cancer cells. miR-490-3p could bind to TNKS2 mRNA 3′UTR directly. miR-490-3p can suppress cell viability and resistance to chemotherapy in colorectal cancer cells through targeting TNKS2. Conclusions miR-490-3p could affect colorectal cancer by targeting TNKS2. This study may provide a potential therapeutic target for colorectal cancer.

scholarly journals MiR 206 inhibits reorganization of the cytoskeleton in melanoma cells by targeting DDX5

2021 ◽  
Vol 20 (11) ◽  
pp. 2279-2285
Author(s):  
Shenglin Wu ◽  
Shan Nie ◽  
Jian Wang
Keyword(s):  
Melanoma Cells ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
M Cells ◽  
Reporter Assay ◽  
Expression Levels ◽  
Invasion And Migration ◽  
Qrt Pcr ◽  
And Migration

Purpose: To investigate the role and mechanism of microRNA-206 (miR-206) in cytoskeleton reorganization in melanoma cells. Methods: MiR-206 and RNA helicase p68 (DDX5) expression levels were measured in A375, A875, and HEM-M cells by quantitative real time polymerase chain reaction (qRT-PCR). A DDX5 overexpression cell line was constructed, and DDX5 overexpression, A375, and A875 cells were transfected with miR-206 mimic or DDX5 small interfering RNA (siRNA). Transwell assay was used to assess cell migration and invasion of A375 and A875 cells, while Luciferase reporter assay was used to determine the putative target of miR-206. DDX5, miR-206, vinculin, coronin3, and ezrin expression levels were evaluated by qRT-PCR. Protein expressions of DDX5, vinculin, coronin3, and ezrin were evaluated by western blot analysis. Results: DDX5 expression was higher and miR-206 expression lower in A375 and A875 cells when compared to HEM-M cells (p < 0.05). Knockdown of DDX5 and overexpression of miR-206 repressed invasion and migration, and inhibited expression of vinculin, coronin3, and ezrin in A375 and A875 cells (p < 0.05). However, overexpression of DDX5 reversed the effect of miR-206 on cytoskeletal protein expression. Luciferase reporter assay data confirmed that DDX5 is a direct target of miR-206 (p < 0.05). Conclusion: MiR-206 suppresses reorganization of the cytoskeleton in melanoma cells by targeting DDX5, and is thus, a promising target for the treatment of melanoma.

scholarly journals miR-375 and miR-205 Regulate the Invasion and Migration of Laryngeal Squamous Cell Carcinoma Synergistically via AKT-Mediated EMT

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Bin Wang ◽  
Kexing Lv ◽  
Weixiong Chen ◽  
Jing Zhao ◽  
Jie Luo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Theoretical Principle ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Qrt Pcr ◽  
And Migration

Previous studies have found that miR-375 and miR-205 were significantly dysregulated in laryngeal squamous cell carcinoma, which contributed to the invasion and migration of LSCC. However, the mechanisms of miR-375 and miR-205 regulating the invasion and migration of LSCC remain unknown. qRT-PCR was performed in 40 pairs of tissue samples to investigate the expression of miR-375 and miR-205 in LSCC and paracarcinoma tissues. To investigate whether or not miR-375 and miR-205 regulated the invasion and migration of LSCC synergistically via AKT-mediated epithelial-mesenchymal transition, miR-375 mimic and miR-205 inhibitor were transfected into SNU899 cells and miR-375 inhibitor and miR-205 mimic were transfected into SNU899 cells, respectively, with or without AKT inhibitor. Then the expressions of miR-375 and miR-205 were validated by qRT-PCR, cell migration and invasion were determined by wound healing assay and transwell invasive assay, and western blot analysis was performed to detect the expression of related proteins. Our results showed that miR-375 and miR-205 regulated the invasion and migration of LSCC via AKT-mediated EMT synergistically. In conclusion, our findings provided not only new information about the molecular mechanism of miRNAs regulating invasion and migration of LSCC, but also a theoretical principle for potential targeting therapy of laryngeal squamous carcinoma.

scholarly journals Mitofusin 2 Expression in Placental Tissues of Preeclamptic Patients and Its Correlations with Trophoblast Invasion and Placental Hypoxia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoyan Wang
Keyword(s):  
Trophoblast Invasion ◽  
Migration And Invasion ◽  
Transwell Assay ◽  
Mitofusin 2 ◽  
Invasion And Migration ◽  
Qrt Pcr ◽  
Protein Expressions ◽  
Normal Women ◽  
And Migration ◽  
Interfering Rna

The researcher aimed to detect mitofusin 2 (Mfn2) expression in the placental tissues of preeclampsia (PE) patients and correlations with trophoblast invasion and placental hypoxia. Mfn2 mRNA expressions in placental tissues from PE and healthy pregnant women were detected by qRT-PCR. Trophoblast cells JEG-3 were transfected with small-interfering RNA-Mfn2 (si-Mfn2). Proliferation was tested by CCK-8 and colony formation assays. Invasion and migration were determined with Transwell assay. Mfn2, HIF-1á, HPH-1 and leptin protein expressions were detected by Western blotting. Mfn2 protein had strong positive and weak negative expressions in normal and PE women, respectively. Mfn2 mRNA expression in PE women was lower than that in normal women (P<0.05). Compared with control and si- NC groups, si-Mfn2 group had lower proliferation, migration and invasion abilities, as well as HIF-1á, HPH-1 and leptin expressions (P<0.05). Mfn2 expression in the placental tissues of PE women obviously decreases, which inhibits trophoblast invasion and triggers placental hypoxia.

Exosomal MicroRNA-325 Enhances Trophoblast Migration and Invasion Through Downregulation of Lethal-7b and Upregulation of Forkhead Box Protein O1 Expression in Preeclampsia

2022 ◽  
Vol 12 (2) ◽  
pp. 248-257
Author(s):  
Ying Xie ◽  
Shan Tian
Keyword(s):  
Trophoblast Cell ◽  
Migration And Invasion ◽  
Tunel Staining ◽  
Trophoblast Cells ◽  
Invasion And Migration ◽  
Forkhead Box ◽  
Cell Progression ◽  
And Migration ◽  
Exosomal Microrna ◽  
Measure Gene Expression

We aimed to explore the mechanism by how microRNA (miRNA)-325 derived from marrow mesenchymal stem cell exosomes (MSC-exos) affects the trophoblast progression in preeclampsia (PE). RT-qPCR detected the level of miRNA let-7b and FOXO1 in the placenta tissue of PE patients. Functional experiment was performed to analyze the effect of FOXO1 inhibitor and let-7b mimics on cell migration, invasion and apoptosis through Transwell assay and TUNEL staining. The trophoblast cell was co-cultured with overexpressed-miR-325 MSC-exos to measure gene expression and cell progression. let-7b was highly and FOXO1 was lowly expressed in PE placenta tissue. let-7b directly targeted and inhibited FOXO1 expression. Importantly, as miR-325 was internalized by trophoblast cells through MSC-exos, MSC-exos overexpressing miR-325 inhibited let-7b expression in trophoblasts, up-regulated FOXO1 and activated AKT signaling pathway. Further, MSC-exos treatment promoted invasion and migration of trophoblast cell and inhibited apoptosis. In conclusion, miR-325 derived from MSC-exos promotes the invasion and migration of trophoblast cells in PE through inhibition of let7b and upregulation of FOXO1.

lncRNA FOXD2-AS1 affects trophoblast cell proliferation, invasion and migration through targeting miRNA

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 131-138 ◽  
Author(s):  
Yulei Zhang ◽  
Xiaoqin Chen
Keyword(s):  
Cell Proliferation ◽  
Matrix Metalloproteinase ◽  
Trophoblast Cell ◽  
Matrix Metalloproteinase 2 ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
Invasion And Migration ◽  
And Migration

SummaryThe abnormal expression of lncRNAs and miRNAs has been found in the placentas of patients with preeclampsia (PE). Therefore, we determined the role of lncRNA FOXD2-AS1/miR-3127 in trophoblast cells. The expression of lncRNA FOXD2-AS1 was detected by qRT-PCR. The proliferation, migration and invasion ability of trophoblast cells were evaluated using CCK-8, wound healing and transwell assays. The target gene of lncRNA FOXD2-AS1 was determined by StarBase and luciferase reporter assays. Western blotting was used to analyze the expression of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9). The results showed that FOXD2-AS1 affected trophoblast cell viability in vitro, while the expression of miR-3127 was decreased. FOXD2-AS1 silencing decreased the promotion effects on trophoblast cell induced by miR-3127 inhibition. In addition, FOXD2-AS1 and miR-3127 presented the same effect on MMP2 and MMP9 levels. lncRNA FOXD2-AS1 modulated trophoblast cell proliferation, invasion and migration through downregulating miR-3127 expression. Therefore, lncRNA FOXD2-AS1 could act as a latent therapeutic marker in preeclampsia.

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