scholarly journals Microarray‑based bioinformatics analysis of the prospective target gene network of key miRNAs influenced by long non‑coding RNA PVT1 in HCC

2018 ◽  
Author(s):  
Yu Zhang ◽  
Wei‑Jia Mo ◽  
Xiao Wang ◽  
Tong‑Tong Zhang ◽  
Yuan Qin ◽  
...  
Keyword(s):  
Gene Network ◽  
Target Gene ◽  
Bioinformatics Analysis ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA MIAT regulates blood tumor barrier permeability by functioning as a competing endogenous RNA

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Jiayuan He ◽  
Yixue Xue ◽  
Qingyuan Wang ◽  
Xinxin Zhou ◽  
Libo Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Target Gene ◽  
Luciferase Assay ◽  
Untranslated Regions ◽  
Brain Drug Delivery ◽  
Combined Application ◽  
Non Coding Rna ◽  
Associated Proteins ◽  
Novel Strategy ◽  
Long Non Coding Rna

Abstract Blood–tumor barrier (BTB) presents a major obstacle to brain drug delivery. Therefore, it is urgent to enhance BTB permeability for the treatment of glioma. In this study, we demonstrated that MIAT, ZAK, and phosphorylated NFκB-p65 (p-NFκB-p65) were upregulated, while miR-140-3p was downregulated in glioma-exposed endothelial cells (GECs) of BTB compared with those in endothelial cells cocultured with astrocytes (ECs) of blood–brain barrier (BBB). MIAT inhibited miR-140-3p expression, increased the expression of ZAK, enhanced the ratio of p-NFκB-p65:NFκB-p65, and promoted the endothelial leakage of BTB. Our current study revealed that miR-140-3p was complementary to the ZAK 3′untranslated regions (3′-UTR), and luciferase activity of ZAK was inhibited by miR-140-3p in 293T cells. MiR-140-3p silencing resulted in an increase in BTB permeability by targeting ZAK, while overexpression of miR-140-3p had the opposite results in GECs of BTB. Overexpression of ZAK induced an increase in BTB permeability, and this effect was related to ZAK’s ability to mediate phosphorylation of NFκB-p65. Conversely, ZAK silencing get opposite results in GECs of BTB. As a molecular sponge of miR-140-3p, MIAT attenuated its negative regulation of the target gene ZAK by adsorbing miR-140-3p. P-NFκB-p65 as a transcription factor negatively regulated the expression of TJ-associated proteins by means of chip assay and luciferase assay. Single or combined application of MIAT and miR-140-3p effectively promoted antitumor drug doxorubicin (Dox) across BTB to induce apoptosis of glioma cells. In summary, MIAT functioned as a miR-140-3p sponge to regulate the expression of its target gene ZAK, which contribution to phosphorylation of NFκB-p65 was associated with an increase in BTB permeability by down-regulating the expression of TJ associated proteins, thereby promoting Dox delivery across BTB. These results might provide a novel strategy and target for chemotherapy of glioma.

scholarly journals Up-regulation of long non-coding RNA SNHG20 promotes ovarian cancer progression via Wnt/β-catenin signaling

2018 ◽  
Vol 38 (1) ◽  
Author(s):  
Shanyang He ◽  
Yunhe Zhao ◽  
Xiaoping Wang ◽  
Yalan Deng ◽  
Zhiyong Wan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Progression ◽  
Target Gene ◽  
Biological Function ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Downstream Target Gene ◽  
Long Non Coding Rna ◽  
Nucleolar Rna ◽  
Signaling Activity

Long non-coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to play crucial regulatory roles in many types of cancer. However, the biological function of long ncRNA (lncRNA) SNHG20 in ovarian cancer is still unclear. In the present study, we found that lncRNA SNHG20 was significantly increased in ovarian cancer. In addition, lncRNA SNHG20 knockdown suppressed the ovarian cancer progression, whereas overexpression of SNHG20 showed the opposite effects. Moreover, our results also revealed that lncRNA SNHG20 knockdown inhibited Wnt/β-catenin signaling activity by suppressing β-catenin expression and reversing the downstream target gene expression. Taken together, lncRNA SNHG20 plays an pivotal role in ovarian cancer progression by regulating Wnt/β-catenin signaling.

scholarly journals Long non-coding RNA MAFG-AS1 promotes proliferation and metastasis of breast cancer by modulating STC2 pathway

2020 ◽  
Author(s):  
Shihao Di ◽  
Die Lu ◽  
Chunni Chen ◽  
Tianshi Ma ◽  
Zigui Zou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Target Gene ◽  
Invasion And Metastasis ◽  
Cancer Proliferation ◽  
Downstream Target ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Downstream Target Gene ◽  
Proliferation And Metastasis ◽  
Long Non Coding Rna

Abstract Objective Breast cancer is the most common cancer in Chinese women. A number of studies proposed that long non-coding RNA plays an essential role in the regulation of invasion and metastasis of various forms of malignancy, including lung cancer, gastric cancer and bladder cancer. In this study, a long non-coding RNA MAFG-AS1 was explored in detail to understand the significance in the etiology of breast cancer.Methods Quantitative reverse transcription PCR (qRT-PCR) was used to examine the expression level of LncRNA MAFG-AS1 in tissues and cell lines. The association of LncRNA MAFG-AS1 expression and the postoperative prognosis was analyzed by the Kaplan-Meier method and log-rank test. Cell proliferation was evaluated in vitro and in vivo . Transwell assays were performed to examine the cell migration. Cell cycle and apoptosis was evaluated by flowcytometry analysis. The downstream target gene STC2 of LncRNA MAFG-AS1 was screened using the microarray analysis, which was validated by qRT-PCR, functional analysis, and rescue experiment.Results Expression of LncRNA MAFG-AS1 in the breast cancer tissues was significantly higher than the precancerous lesions. Elevated expression level of LncRNA MAFG-AS1 was correlated to the larger GTV (gross tumor volume), negative expression of ER, PR, Her2, lymph node metastasis, and poor prognosis. The potency of breast cancer proliferation, invasion and metastasis was inhibited in the absence of LncRNA MAFG-AS1.Tumorigenic capacity of breast cancer cells was inhibited in the absence of LncRNA MAFG-AS1. The downstream target gene regulated by LncRNA MAFG-AS1 was screened out by gene chip technology, GO analysis and QRT-PCR ultimately. Disrupted STC2 suppressed the cell proliferation and metastasis when the level of LncRNA MAFG-AS1 elevated.Conclusion The LncRNA MAFG-AS1 triggers tumorigenesis in the breast cancer and regulates breast cancer proliferation and metastasis by modulating the downstream target gene STC2. Results from our study indicates that LncRNA MAFG-AS1 can be used.

Long non-coding RNA tumor protein 53 target gene 1 promotes cervical cancer development via regulating microRNA-33a-5p to target forkhead box K2 (Preprint)

2021 ◽  
Author(s):  
Yanyan Liu Sr ◽  
xiaomei Liu ◽  
xiuying Yuan ◽  
poling Feng ◽  
zhiwei Ouyang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Target Gene ◽  
Mtor Signaling ◽  
Regulatory Function ◽  
Clinical Samples ◽  
Mtor Signaling Pathway ◽  
Forkhead Box ◽  
Non Coding Rna ◽  
Long Non Coding Rna

BACKGROUND Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been studied in multiple diseases, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p to target Forkhead box K2 (FOXK2) remains limited. This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. OBJECTIVE This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. METHODS The clinical samples were collected and TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 and miR-33a-5p to determine the change of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. RESULTS TP53TG1 and FOXK2 were enriched and miR-33a-5p was inhibited in CC. The reduced TP53TG1 or FOXK2 or elevated miR-33a-5p decelerated the CC cell development and the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or enriched miR-33a-5p reversed the effects of decreased TP53TG1. TP53TG1 sponged miR-33a-5p which targeted FOXK2. The experiment in vivo validated the outcomes of the experiment in vitro. CONCLUSIONS TP53TG1 accelerates the CC development via regulating miR-33a-5p to target FOXK2 with the involvement of PI3K/AKT/mTOR signaling pathway. This study provides novel theory references and a distinct direction for the therapy strategies of CC.

scholarly journals LncRNA TUG1 Regulates Proliferation of Cardiac Fibroblast via the miR-29b-3p/TGF-β1 Axis

2021 ◽  
Vol 8 ◽  
Author(s):  
Yini Guo ◽  
Zongli Sun ◽  
Minghe Chen ◽  
Junjie Lun
Keyword(s):  
Target Gene ◽  
Cardiac Fibroblasts ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Healthy Controls ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Taurine Upregulated Gene 1 ◽  
Tgf Β1

Background: Atrial fibrillation (AF) is a very common clinical arrhythmia, accompanied by the overproliferation of cardiac fibroblasts (CFs). This study aimed to investigate the role of the long non-coding RNA(lncRNA) taurine upregulated gene 1 (TUG1) in the proliferation of CFs and further investigated its underlying mechanism.Methods: One hundred four paroxysmal AF patients and 94 healthy controls were recruited. Human cardiac fibroblasts (HCFs) were applied to establish an AF cell model through treatment with angiotensin II (AngII). qRT-PCR was used for the measurement of gene levels. The cell proliferation was detected by cell counting kit-8 (CCK-8). Luciferase reporter assay was performed for target gene analysis.Results: Elevated levels of TUG1 and low expression of miR-29b-3p were detected in the serum of AF patients compared with the healthy controls. Pearson's correlation analysis exhibited an inverse relationship between TUG1 and miR-29b-3p expression in AF patients (r = −7.106, p < 0.001). Knockdown of TUG1 inhibited AngII-induced CF proliferation. Taurine upregulated gene 1 (TUG1) functions as a competing endogenous RNA (ceRNA) for miR-29b-3p, and downregulation of miR-29b-3p reversed the role of TUG1 in CF proliferation. TGF-β1 is a direct target gene of miR-29b-3p.Conclusions: Long non-coding RNA taurine upregulated gene 1 is a key regulator in the occurrence of AF. Slicing TUG1 inhibits CF proliferation by regulating the miR-29b-3p/TGF-β1 axis.

scholarly journals A Human Long Non-Coding RNA ALT1 Controls the Cell Cycle of Vascular Endothelial Cells Via ACE2 and Cyclin D1 Pathway

2017 ◽  
Vol 43 (3) ◽  
pp. 1152-1167 ◽  
Author(s):  
Wen Li ◽  
Rui Wang ◽  
Jie-yi Ma ◽  
Mian Wang ◽  
Jin Cui ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Cyclin D1 ◽  
Target Gene ◽  
Vascular Endothelial Cells ◽  
Lymphocytic Leukemia ◽  
Mass Spectrometry Analysis ◽  
Vascular Endothelial ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Background/Aims: ALT1 is a novel long non-coding RNA derived from the alternatively spliced transcript of the deleted in lymphocytic leukemia 2 (DLEU2). To date, ALT1 biological roles in human vascular endothelial cells have not been reported. Methods: ALT1 was knocked down by siRNAs. Cell proliferation was analyzed by cck-8. The existence and sequence of human ALT1 were identified by 3’ rapid amplification of cDNA ends. The interaction between lncRNA and proteins was analyzed by RNA-Protein pull down assay, RNA immunoprecipitation, and mass spectrometry analysis. Results: ALT1 was expressed in human umbilical vein endothelial cells (HUVECs). The expression of ALT1 was significantly downregulated in contact-inhibited HUVECs and in hypoxia-induced, growth-arrested HUVECs. Knocking down of ALT1 inhibited the proliferation of HUVECs by G0/G1 cell cycle arrest. We observed that angiotensin converting enzyme Ⅱ(ACE2) was a direct target gene of ALT1. Knocking-down of ALT1 or its target gene ACE2 could efficiently decrease the expression of cyclin D1 via the enhanced ubiquitination and degradation, in which HIF-1α and protein von Hippel-Lindau (pVHL) might be involved. Conclusion: The results suggested the human long non-coding RNA ALT1 is a novel regulator for cell cycle of HUVECs via ACE2 and cyclin D1 pathway.

scholarly journals Identification of Potential Prognostic Long Non-Coding RNA Biomarkers for Predicting Survival in Patients with Hepatocellular Carcinoma

2018 ◽  
Vol 48 (5) ◽  
pp. 1854-1869 ◽  
Author(s):  
Xiwen Liao ◽  
Chengkun Yang ◽  
Rui Huang ◽  
Chuangye Han ◽  
Tingdong Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Functional Assessment ◽  
Bioinformatics Analysis ◽  
Survival Prediction ◽  
Prognostic Signature ◽  
Characteristic Analysis ◽  
Risk Of Death ◽  
Non Coding Rna ◽  
Cox Analysis ◽  
Long Non Coding Rna

Background/Aims: The aim of the current study was to identify potential prognostic long non-coding RNA (lncRNA) biomarkers for predicting survival in patients with hepatocellular carcinoma (HCC) using The Cancer Genome Atlas (TCGA) dataset and bioinformatics analysis. Methods: RNA sequencing and clinical data of HCC patients from TCGA were used for prognostic association assessment by univariate Cox analysis. A prognostic signature was built using stepwise multivariable Cox analysis, and a comprehensive analysis was performed to evaluate its prognostic value. The prognostic signature was further evaluated by functional assessment and bioinformatics analysis. Results: Thirteen differentially expressed lncRNAs (DELs) were identified and used to construct a single prognostic signature. Patients with high risk scores showed a significantly increased risk of death (adjusted P < 0.0001, adjusted hazard ratio = 3.522, 95% confidence interval = 2.307–5.376). In the time-dependent receiver operating characteristic analysis, the prognostic signature performed well for HCC survival prediction with an area under curve of 0.809, 0.782 and 0.79 for 1-, 3- and 5-year survival, respectively. Comprehensive survival analysis of the 13-DEL prognostic signature suggested that it serves as an independent factor in HCC, showing a better performance for prognosis prediction than traditional clinical indicators. Functional assessment and bioinformatics analysis suggested that the prognostic signature was associated with the cell cycle and peroxisome proliferator-activated receptor signaling pathway. Conclusions: The novel lncRNA expression signature identified in the present study may be a potential biomarker for predicting the prognosis of HCC patients.

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