scholarly journals Downregulation of LncRNA-MEG3 promotes HTR8/SVneo cells apoptosis and attenuates its migration by repressing Notch1 signal in preeclampsia

Reproduction ◽  
2020 ◽  
Vol 160 (1) ◽  
pp. 21-29
Author(s):  
Rongli Wang ◽  
Li Zou
Keyword(s):  
Cell Migration ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Function ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Trophoblast Cells

A successful pregnancy crucially depends on well-regulated extravillous trophoblast migration and invasion. Maternally expressed gene 3 (MEG3) is a long noncoding RNA that plays an important role in regulating trophoblast cells cell function. As previously reported, the expression of MEG3 was reduced in preeclampsia, and downregulation of MEG3 could suppress trophoblast cells migration and promote its apoptosis. However, the downstream regulatory mechanism of MEG3 remains unknown. As reported, MEG3 could inhibit cell proliferation in endometrial carcinoma by regulating Notch signaling. Our previous studies have demonstrated that Notch1 is downregulated in preeclampsia and that inhibiting the expression of Notch1 could promote trophoblast cell apoptosis. Therefore, this study was designed to investigate the role of MEG3 and its the relationship with Notch1 in trophoblasts. In this study, the mRNA expression levels of both MEG3 and Notch1 were decreased in preeclampsia placenta (n = 15) compared to the normal samples (n = 15). Exogenous upregulation and downregulation of MEG3 in HTR8/SVneo cells were performed to investigate the role of MEG3 in cell biological behavior and its effects on Notch1 expression. The results showed that MEG3 enhancement promoted trophoblast cell migration and invasion and inhibited cell apoptosis. Downregulation of MEG3 elicited the opposite results. Associated factors, such as matrix metalloproteinases 2 (MMP2), BAX, and Bcl-2, were examined at the mRNA and protein levels. Our study demonstrated that MEG3 could regulate Notch1 expression to modulate trophoblast cell migration, invasion, and apoptosis, which may represent the molecular mechanism of poor placentation during preeclampsia.

scholarly journals Long noncoding RNA TTN-AS1 promotes breast cancer cell migration and invasion via sponging miR-140-5p

2020 ◽  
Author(s):  
Yusheng Li ◽  
Fan Wang
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Noncoding Rna ◽  
Vital Role ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Behavior Changes ◽  
Cell Migration And Invasion ◽  
Rna Immunoprecipitation

Abstract Objectives Breast cancer (BC) is one of the most ordinary fatal cancers. Recent studies have identified the vital role of long noncoding RNAs (lncRNAs) in the development and progression of BC. In this research, lncRNA TTN-AS1 was studied to identify how it functioned in the metastasis of BC.Methods TTN-AS1 expression of tissues was detected by RT-qPCR in 56 BC patients. Wound healing assay and transwell assay were used to observe the biological behavior changes of BC cells through gain or loss of TTN-AS1. In addition, luciferase assays and RNA immunoprecipitation (RIP) assay were performed to discover the potential targets of TTN-AS1 in BC cells.Results TTN-AS1 expression level in BC samples was higher than that of adjacent ones. Besides, cell migrated ability and cell invaded ability of BC cells were inhibited after TTN-AS1 was silenced. Cell migrated ability and cell invaded ability of BC cells were promoted after TTN-AS1 was overexpressed. In addition, miR-140-5p was upregulated after silence of TTN-AS1 in BC cells, while miR-140-5p was downregulated after overexpression of TTN-AS1 in BC cells. Furthermore, luciferase assays and RNA immunoprecipitation assay (RIP) showed that miR-140-5p was a direct target of TTN-AS1 in BC.Conclusion Our study uncovers a new oncogene in BC and suggests that TTN-AS1 could enhance BC cell migration and invasion via sponging miR-140-5p, which provides a novel therapeutic target for BC patients.

Vaccinium angustifolium (lowbush blueberry) leaf extract increases extravillous trophoblast cell migration and invasion in vitro

2018 ◽  
Vol 32 (4) ◽  
pp. 705-714 ◽  
Author(s):  
Christina Ly ◽  
Jonathan Ferrier ◽  
Jeremiah Gaudet ◽  
Julien Yockell-Lelièvre ◽  
John Thor Arnason ◽  
...  
Keyword(s):  
Cell Migration ◽  
Leaf Extract ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast ◽  
Migration And Invasion ◽  
Vaccinium Angustifolium ◽  
Cell Migration And Invasion ◽  
Lowbush Blueberry

scholarly journals Acyl-CoA Synthetase 5 Promotes the Growth and Invasion of Colorectal Cancer Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Shihua Ding ◽  
Shaohui Tang ◽  
Min Wang ◽  
Donghai Wu ◽  
Haijian Guo
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Sw620 Cells ◽  
Role Of It

Background and Aims. Acyl-CoA synthetase 5 (ACS5) has been reported to be associated with the development of various cancers, but the role of it in colorectal cancer (CRC) is not well understood. The present study aimed to explore the potential role of ACS5 in the development and progression of CRC. Methods. ACS5 expression in CRC tissues and CRC cell lines was examined, and its clinical significance was analyzed. The role of ACS5 in cell proliferation, apoptosis, and invasion was examined in vitro. Results. We found that ACS5 expression was upregulated in CRC cells and CRC tissues and that high ACS5 expression was more frequent in CRC patients with excess muscular layer and with poor tumor differentiation. Furthermore, knockdown of ACS5 in HT29 and SW480 cells significantly dampened cell proliferation, induced cell apoptosis, and reduced cell migration and invasion. In contrast, the ectopic overexpression of ACS5 in LOVO and SW620 cells remarkably promoted cell proliferation, inhibited cell apoptosis, and enhanced cell migration and invasion. Enhanced cell growth and invasion ability mediated by the gain of ACS5 expression were associated with downregulation of caspase-3 and E-cadherin and upregulation of survivin and CD44. Conclusions. Our data demonstrate that ACS5 can promote the growth and invasion of CRC cells and provide a potential target for CRC gene therapy.

scholarly journals Effects of Human Umbilical Cord Mesenchymal Stem Cells on Human Trophoblast Cell Functions In Vitro

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Yajing Huang ◽  
Yanming Wu ◽  
Xinwen Chang ◽  
Yan Li ◽  
Kai Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Cell Function ◽  
Trophoblast Cell ◽  
Migration And Invasion ◽  
Human Umbilical Cord ◽  
Trophoblast Cells ◽  
Human Trophoblast ◽  
Cell Functions

Trophoblast cell dysfunction is involved in many disorders during pregnancy such as preeclampsia and intrauterine growth restriction. Few treatments exist, however, that target improving trophoblast cell function. Human umbilical cord mesenchymal stem cells (hUCMSCs) are capable of self-renewing, can undergo multilineage differentiation, and have homing abilities; in addition, they have immunomodulatory effects and paracrine properties and thus are a prospective source for cell therapy. To identify whether hUCMSCs can regulate trophoblast cell functions, we treated trophoblast cells with hUCMSC supernatant or cocultured them with hUCMSCs. Both treatments remarkably enhanced the migration and invasion abilities of trophoblast cells and upregulated their proliferation ability. At a certain concentration, hUCMSCs also modulated hCG, PIGF, and sEndoglin levels in the trophoblast culture medium. Thus, hUCMSCs have a positive effect on trophoblast cellular functions, which may provide a new avenue for treatment of placenta-related diseases during pregnancy.

scholarly journals PM10 Alters Trophoblast Cell Function and Modulates miR-125b-5p Expression

2022 ◽  
Vol 2022 ◽  
pp. 1-11
Author(s):  
Wittaya Chaiwangyen ◽  
Komsak Pintha ◽  
Payungsak Tantipaiboonwong ◽  
Piyawan Nuntaboon ◽  
Orawan Khantamat ◽  
...  
Keyword(s):  
Mirna Expression ◽  
Cell Function ◽  
Premature Mortality ◽  
Trophoblast Cell ◽  
Migration And Invasion ◽  
Trophoblast Cells ◽  
High Concentration ◽  
Particulate Pollution ◽  
Cell Functions ◽  
Pollution Exposure

Air pollution is one of the largest global environmental health hazards that threaten premature mortality or morbidity. Particulate matter 10 (PM10) has been demonstrated to contribute to several human diseases via dysregulated miRNA expression. Trophoblast cells play a key role in implantation and placentation for a successful pregnancy. Nonetheless, the PM10 associated trophoblast cell functions during pregnancy and miRNA expression are still unknown. Our study showed that PM10 affected HTR-8/SVneo cell viability and also decreased cell proliferation, migration, and invasion. A high concentration of PM10 caused an increase in HTR-8/SVneo cell apoptosis. Treatment with PM10 induced inflammation through the upregulated IL-1β, IL-6, and TNF-α expression in trophoblast cells. In PM10-treated HTR-8/SVneo cells, miR-125b-5p expression was considerably increased and TXNRD1 was found to be negatively related to miR-125b-5p. Collectively, our findings revealed that PM10 could alter miR-125b-5p expression by targeting TXNRD1 and suppressing trophoblast cell functions. Additional investigations relating to the function of miR-125b-5p and its target on particulate pollution exposure in trophoblast are warranted for future biomarker or effective therapeutic approaches.

scholarly journals Long Noncoding RNA SOX2-OT Exacerbates Hypoxia-Induced Cardiomyocytes Injury by Regulating miR-27a-3p/TGFβR1 Axis

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Guang Yang ◽  
Chunsheng Lin
Keyword(s):  
Heart Failure ◽  
Cell Apoptosis ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Heart Diseases ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cellular Processes ◽  
Wide Range

Background. Myocardial infarction (MI) was a severe cardiovascular disease resulted from acute, persistent hypoxia, or ischemia condition. Additionally, MI generally led to heart failure, even sudden death. A multitude of research studies proposed that long noncoding RNAs (lncRNAs) frequently participated in the regulation of heart diseases. The specific function and molecular mechanism of SOX2-OT in MI remained unclear. Aim of the Study. The current research was aimed to explore the role of SOX2-OT in MI. Methods. Bioinformatics analysis (DIANA tools and Targetscan) and a wide range of experiments (CCK-8, flow cytometry, RT-qPCR, luciferase reporter, RIP, caspase-3 activity, trans-well, and western blot assays) were adopted to investigate the function and mechanism of SOX2-OT. Results. We discovered that hypoxia treatment decreased cell viability but increased cell apoptosis. Besides, lncRNA SOX2-OT expression was upregulated in hypoxic HCMs. Hereafter, we confirmed that SOX2-OT could negatively regulate miR-27a-3p levels by directly binding with miR-27a-3p, and miR-27a-3p also could negatively regulate SOX2-OT levels. Furthermore, knockdown of SOX2-OT promoted cell proliferation, migration, and invasion, but limited cell apoptosis. However, these effects were reversed by anti-miR-27a-5p. Besides, we verified that miR-27a-3p binding with the 3′UTR of TGFBR1 and SOX2-OT regulated TGFβR1 level by collaborating with miR-27a-3p in HCMs. Eventually, rescue assays validated that the influence of SOX2-OT silence or miR-27a-3p overexpression on cellular processes in cardiomyocytes injury was counteracted by TGFBR1 overexpression. Conclusions. Long noncoding RNA SOX2-OT exacerbated hypoxia-induced cardiomyocytes injury by regulating miR-27a-3p/TGFβR1 axis, which may provide a novel insight for heart failure treatment.

scholarly journals The regulatory role of peripheral blood mononuclear cell function by A20

2020 ◽  
Vol 17 (4) ◽  
pp. 603-609
Author(s):  
Nguyen Thi Xuan ◽  
Nguyen Huy Hoang
Keyword(s):  
Cell Migration ◽  
Peripheral Blood ◽  
Cell Apoptosis ◽  
Mononuclear Cells ◽  
Cell Function ◽  
Binding Capacity ◽  
Negative Regulator ◽  
Peripheral Blood Mononuclear ◽  
Migration Assay

Peripheral blood mononuclear cells (PBMC) consist of lymphocytes (T cells, B cells, natural killer cells), monocytes and dendritic cells and play important roles in initiating and regulating immunity against pathogens or immunotolerance to allergens. Activation of PBMCs is induced upon exposure to multiple stimuli by the binding with toll-like receptors (TLRs), recognition elements of the innate immune system. A20 is a negative regulator of nuclear factor (NF)-κB-dependent immune reaction in response to TLR ligands. A20-deficient mice display severe inflammation, tissue damage in multiple organs, cachexia and premature mortality. Single nucleotide polymorphisms (SNPs) at A20 gene region in humans reduce the binding capacity of A20 to NF‐κB subunits, resulting in reduced expression and function of A20 and leading to the pathogenesis of autoimmune and cancers. Although the inhibitory role of A20 on immune cells including B, T and DC functions has been previously reported, the effect of A20 on PBMC function is not mentioned yet. The present study, therefore, explored whether A20 expression is involved in immunophenotypic changes, the release of cytokine production, cell migration, and apoptosis. To this end, immonophenotypic profile and cell apoptosis were examined by flow cytometry, secretion of inflammatory cytokines by ELISA and cell migration by a transwell migration assay. As a result, percentages of CD3+CD25+, CD19+CD25+, and CD11b+CD40+ expressing cells, the release of TNF-α and IL-1β and cell migration were enhanced in A20-silenced PBMCs. However, cell apoptosis was independent of the presence of A20 in PBMCs. In conclusion, these results attained in this study suggested that A20 expression might modulate the immune response in autoimmune disease and cancers.

scholarly journals Upregulation of circRNA hsa_circ_0008726 in Pre-eclampsia Inhibits Trophoblast Migration, Invasion, and EMT by Regulating miR-345-3p/RYBP Axis

2021 ◽  
Author(s):  
Chang Shu ◽  
Peng Xu ◽  
Jun Han ◽  
Shumei Han ◽  
Jin He
Keyword(s):  
Cell Migration ◽  
Epithelial Mesenchymal Transition ◽  
Extravillous Trophoblast ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Rnase R ◽  
Mesenchymal Transition ◽  
Potential Biomarker ◽  
Rna Immunoprecipitation

AbstractAccumulating evidence shows that impaired spiral artery remodeling, placental dysfunction, and insufficient trophoblast infiltration contribute to the etiology and pathogenesis of pre-eclampsia (PE). circRNAs are a class of endogenous non-coding RNAs implicated in the pathogenesis of many diseases, including PE. This study aims to investigate the role of circRNA hsa_circ_0008726 in regulating the migration and invasion of extravillous trophoblast cells. RNase R assay was performed to confirm that circ_0008726 was a circular transcript. The expression of circ_0008726, RYBP, and miR-345-3p was examined by qRT-PCR. The functional interaction between miR-345-3p and circ_0008726 or RYBP was confirmed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Cell migration and invasion ability was analyzed by Transwell assays. Western blot was used for the quantification of RYBP protein level. Circ_0008726 expression was significantly increased in PE placenta tissues as compared with normal placenta tissues. Circ_0008726 was resistant to RNase R digestion and was predominately located in the cytoplasm of HTR-8/SVneo cells. Silencing circ_0008726 promoted cell migration and EMT (epithelial-mesenchymal transition), while circ_0008726 overexpression suppressed these processes. Mechanistically, circ_0008726 sponged miR-345-3p to negatively regulate its expression, and miR-345-3p negatively modulated the expression of RYBP. In PE samples, the expression level of circ_0008726 was negatively correlated with miR-345-3p level, but was positively correlated with RYBP expression. Transfection of miR-345-3p mimic or RYBP knockdown counteracted the effects of circ_0008726 overexpression on cell migration and EMT. Our data demonstrate the upregulation of circ_0008726 in PE placenta, which inhibits the migration, invasion, and EMT of HTR-8/SVneo cells by targeting miR-345-3p/RYBP axis. These data suggest that circ_0008726 could be a potential biomarker and therapeutic target for PE.

Role of growth factors and other placental signals in extravillous trophoblast cell function

Placenta ◽  
1998 ◽  
Vol 19 ◽  
pp. 327-339
Author(s):  
Peeyush K. Lala ◽  
G. Scot Hamilton ◽  
Andrew Athanassiades
Keyword(s):  
Growth Factors ◽  
Cell Function ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast
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