The lncRNA small nucleolar RNA host gene 5 regulates trophoblast cell proliferation, invasion, and migration via modulating miR‐26a‐5p/N‐cadherin axis

2018 ◽  
Vol 120 (3) ◽  
pp. 3173-3184 ◽  
Author(s):  
Yang Yang ◽  
Lan Xi ◽  
Yuan Ma ◽  
Xiaoming Zhu ◽  
Rui Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Trophoblast Cell ◽  
Host Gene ◽  
Small Nucleolar Rna ◽  
Invasion And Migration ◽  
And Migration ◽  
Nucleolar Rna

Circ_0085296 suppresses trophoblast cell proliferation, invasion, and migration via modulating miR-144/E-cadherin axis

Placenta ◽  
2020 ◽  
Vol 97 ◽  
pp. 18-25
Author(s):  
Hailing Zhu ◽  
Xia Niu ◽  
Qinghua Li ◽  
Yuehua Zhao ◽  
Xue Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Trophoblast Cell ◽  
Invasion And Migration ◽  
And Migration ◽  
E Cadherin

scholarly journals lncRNA small nucleolar RNA host gene 20 predicts poor prognosis in glioma and promotes cell proliferation by silencing P21

2019 ◽  
Vol Volume 12 ◽  
pp. 805-814 ◽  
Author(s):  
Xiang-Sheng Li ◽  
Fa-Zheng Shen ◽  
Li-Yong Huang ◽  
Lei Hui ◽  
Rui-Hua Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Poor Prognosis ◽  
Host Gene ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna

scholarly journals Long Non-coding RNA Small Nucleolar RNA Host Gene 14, a Promising Biomarker and Therapeutic Target in Malignancy

2021 ◽  
Vol 9 ◽  
Author(s):  
Shen Shen ◽  
Yanfang Wang ◽  
Yize Zhang ◽  
Zihui Dong ◽  
Jiyuan Xing
Keyword(s):  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Clinicopathological Characteristics ◽  
Host Gene ◽  
Loss Of Function ◽  
Small Nucleolar Rna ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Nucleolar Rna

Small nucleolar RNA host gene 14 (SNHG14) is a long non-coding RNA found to be overexpressed in various types of cancers. Moreover, the expression level of SNHG14 was closely associated with multiple clinicopathological characteristics such as prognosis, tumor differentiation, TNM stage, and lymph node metastasis. Functionally, gain- and loss-of-function of SNHG14 revealed that overexpressed SNHG14 promoted cancer cell viability, invasion, and migration, whereas its down-regulation produced the opposite effect. Mechanistically, regulating its target gene expression by sponging distinct miRNAs might be the major mechanism underlying the oncogenic functions of SNHG14. Thus, SNHG14 might be a promising prognostic biomarker and therapeutic target for cancers. In this review, we discuss the expression profile, biological function, and molecular mechanisms of SNHG14 in cancers to provide a molecular basis for the clinical utility of SNHG14 in the future.

scholarly journals Expression and gene regulatory network of SNHG1 in hepatocellular carcinoma

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Chaoran Zheng ◽  
Shicheng Yu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Regulatory Network ◽  
Noncoding Rna ◽  
Host Gene ◽  
P Value ◽  
Tumour Suppressor Genes ◽  
Sequencing Data ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna

Abstract Background Small nucleolar RNA host gene 1 (SNHG1), a long noncoding RNA (lncRNA), is a transcript that negatively regulates tumour suppressor genes, such as p53. Abnormal SNHG1 expression is associated with cell proliferation and cancer. We used sequencing data downloaded from Genomic Data Commons to analyse the expression and interaction networks of SNHG1 in hepatocellular carcinoma (HCC). Methods Expression was examined using the limma package of R and verified by Gene Expression Profiling Interactive Analysis. We also obtained miRNA expression data from StarBase to determine the lncRNA-miRNA-mRNA–related RNA regulatory network in HCC. Kaplan–Meier (KM) analysis was performed using the survival package of R. Gene Ontology annotation of genes was carried out using Metascape. Results We found that SNHG1 was overexpressed and often amplified in HCC patients. In addition, SNHG1 upregulation was associated with the promotion of several primary biological functions, including cell proliferation, transcription and protein binding. Moreover, we found similar trends of small nucleolar RNA host gene 1 (SNHG1), E2F8 (E2F transcription factor 8), FANCE (FA complementation group E) and LMNB2 (encodes lamin B2) expression. In the SNHG1-associated network, high expression levels of SNHG1 (log-rank P value = 0.0643), E2F8 (log-rank P value = 0.000048), FANCE (log-rank P value = 0.00125) and LMNB2 (log-rank P value = 0.0392) were significantly associated with poor survival. Single-cell analysis showed that E2F8 may play an important role in tumorigenesis or cancer development. Conclusions Our results highlight the benefit of utilizing multiple datasets to understand the functional potential regulatory networks of SNHG1 and the role of SNHG1 in tumours.

Long Noncoding RNA Small Nucleolar RNA Host Gene 6 Promotes Cell Proliferation, Migration and Invasion in Melanoma by Sponging miR-944

2021 ◽  
Vol 11 (8) ◽  
pp. 1459-1465
Author(s):  
Jinjin Zhu ◽  
Pan Xu
Keyword(s):  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Melanoma Cells ◽  
Host Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna ◽  
A375 Cells

Long noncoding RNA small nucleolar RNA host gene 6 (SNHG6) has been reported to be a tumor promoter in various human cancers. Nevertheless, the detailed functions and clinical value of SNHG6 in melanoma remain elusive. The study aimed to investigate the role and potential mechanism of SNHG6 in melanoma metastasis. Quantitative real-time PCR (qRT-PCR) was used to detect the expressions of SNHG6 and miR-944 in melanoma cells. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, and cell migration and invasion were measured by wound healing assay and cell invasion assay, respectively. In addition, dual luciferase reporter assay was performed to verify the interaction between SNHG6 and miR-944. The protein expressions of PI3K/Akt pathway were evaluated by western blot assay. The results revealed that SNHG6 expression was significantly increased in melanoma cells. Knockdown of SNHG6 suppressed cell proliferation, migration and invasion in A375 cells. Moreover, miR-944 was identified as a direct target of SNHG6 in melanoma. miR-944 was downregulated in melanoma cells, while SNHG6 silencing improved miR-944 level in A375 cells. Rescue experiments demonstrated that miR-944 overexpression reversed the effects of SNHG6 on A375 cell proliferation, migration and invasion. Altogether, SNHG6 exerted oncogenic effects in melanoma cells, providing a novel promising target for the treatment of melanoma.

scholarly journals The Increased lncRNA MIR503HG in Preeclampsia Modulated Trophoblast Cell Proliferation, Invasion, and Migration via Regulating Matrix Metalloproteinases and NF-κB Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Dan Cheng ◽  
Shan Jiang ◽  
Jiao Chen ◽  
Jie Li ◽  
Liangfei Ao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Western Blot ◽  
Trophoblast Cell ◽  
Migration Flow ◽  
Expression Levels ◽  
Invasion And Migration ◽  
And Migration

Background. Preeclampsia (PE) is a pregnancy-related syndrome characterized by hypertension and proteinuria after the 20th week of gestation. The long noncoding RNAs (lncRNAs) have been recently discovered for their roles in the pathogenesis of PE. This study is aimed at determining the expression of lncRNA MIR503 host gene (MIR503HG) in PE placental tissues and exploring the molecular mechanism underlying MIR503HG-mediated trophoblast cell proliferation, invasion, and migration. Methods. The expression level of MIR503HG in placental tissues, HTR-8/SVneo, and JEG3 cells was determined by quantitative real-time PCR; western blot detected the relevant protein expression levels in HTR-8/SVneo and JEG3 cells; flow cytometry determined cell apoptosis and cell cycle of HTR-8/SVneo and JEG3 cells; trophoblast cell proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells were measured by CCK-8, transwell invasion, and wound healing assays, respectively. Results. The highly expressed MIR503HG was detected in PE placental tissues compared to normal placental tissues. MIR503HG overexpression suppressed cell proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells, while knockdown of MIR503HG increased trophoblast cell proliferation, invasion, and migration. Flow cytometry results showed that MIR503HG overexpression induced apoptosis and caused cell cycle arrest at the G0/G1 phase, while MIR503HG knockdown had the opposite actions in HTR-8/SVneo and JEG3 cells. Western blot assay results showed that MIR503HG overexpression suppressed the matrix metalloproteinase-2/-9 and the snail protein expression and increased the E-cadherin expression in trophoblast cells. In addition, MIR503HG overexpression suppressed the NF-κB signaling pathway by inhibiting the phosphorylation of IκBα and the nuclear translocation of NF-κB signaling subunit p65. On the other hand, MIR503HG knockdown played an opposite role in these protein expression levels. Conclusion. Our results showed that MIR503HG inhibited the proliferation, invasion, and migration of HTR-8/SVneo and JEG3 cells, which may be related to the pathogenesis of PE.

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.

scholarly journals YB-1 Is Altered in Pregnancy-Associated Disorders and Affects Trophoblast in Vitro Properties via Alternation of Multiple Molecular Traits

2021 ◽  
Vol 22 (13) ◽  
pp. 7226
Author(s):  
Violeta Stojanovska ◽  
Aneri Shah ◽  
Katja Woidacki ◽  
Florence Fischer ◽  
Mario Bauer ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Progression ◽  
Cell Function ◽  
Trophoblast Cell ◽  
Mrna Levels ◽  
Trophoblast Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Apoptosis And Inflammation

Cold shock Y-box binding protein-1 (YB-1) coordinates several molecular processes between the nucleus and the cytoplasm and plays a crucial role in cell function. Moreover, it is involved in cancer progression, invasion, and metastasis. As trophoblast cells share similar characteristics with cancer cells, we hypothesized that YB-1 might also be necessary for trophoblast functionality. In samples of patients with intrauterine growth restriction, YB-1 mRNA levels were decreased, while they were increased in preeclampsia and unchanged in spontaneous abortions when compared to normal pregnant controls. Studies with overexpression and downregulation of YB-1 were performed to assess the key trophoblast processes in two trophoblast cell lines HTR8/SVneo and JEG3. Overexpression of YB-1 or exposure of trophoblast cells to recombinant YB-1 caused enhanced proliferation, while knockdown of YB-1 lead to proliferative disadvantage in JEG3 or HTR8/SVneo cells. The invasion and migration properties were affected at different degrees among the trophoblast cell lines. Trophoblast expression of genes mediating migration, invasion, apoptosis, and inflammation was altered upon YB-1 downregulation. Moreover, IL-6 secretion was excessively increased in HTR8/SVneo. Ultimately, YB-1 directly binds to NF-κB enhancer mark in HTR8/SVneo cells. Our data show that YB-1 protein is important for trophoblast cell functioning and, when downregulated, leads to trophoblast disadvantage that at least in part is mediated by NF-κB.

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