LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE178402 | GEO | 2024/06/17
REPOSITORIES: GEO
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Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
2024-06-17 | GSE178401 | GEO
Project description:In the current study, on the basis of establishment of PA-induced damage model of HUVECs, the silencing and overexpression (OE) of HIF1A-AS1 were implemented in the HUVECs, and the effects on cell viability, apoptosis, migration and invasion were explored, respectively. Functionally, the results indicated silencing of HIF1A-AS1 promoted the proliferation migration and invasion, and reduced the apoptosis of HUVECs. In contrast, OE of HIF1A-AS1 reduced proliferation transwell and invasion, promoted the apoptosis, suggesting that HIF1A-AS1 play vital roles in regulating HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were carried out, and the results indicated that HIF1A-AS1 globally mediate expression of miRNA and mRNA. The multiple target genes of DEmiRNA were associated with cell proliferation and apoptosis, and overlapped with the DEGs from RNA-seq, suggestion that HIF1A-AS1 might regulate the proliferation and apoptosis of HUVECs by regulating miRNA expression.
2024-06-17 | GSE178397 | GEO
Project description:LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression
| PRJNA738878 | ENA
Project description:LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression [miRNA-Seq]
| PRJNA738875 | ENA
Project description:LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression [RNA-Seq]
| PRJNA738885 | ENA
Project description:Chronic hepatitis B virus infection is a major risk factor for hepatocellular carcinoma. HBV infection affects lncRNA expression in infected cells, but the detailed mechanism and biological significance are not yet clear. In this study, we focused on exploring the function of the HBV-upregulated lncRNA SAMD12-AS1 in cell proliferation. We found that there is a higher level of SAMD12-AS1 expression in tumors than in adjacent nontumorous liver tissues. We showed that ectopic expression of SAMD12-AS1 promotes cell growth and blocks apoptosis, while knockdown of SAMD12-AS1 inhibits cell proliferation and enhances etoposide-induced apoptosis. Using RNA immunoprecipitation and mass spectrometry, we determined that SAMD12-AS1 interacts with NPM1 and confirmed that SAMD12-AS1(1-350) is required for the interaction with NPM1. As it is known that NPM1 interacts with the E3 ligase HDM2 and reduces HDM2-mediated p53 degradation, we examined whether SAMD12-AS1 can affect p53 stability. Overexpression of SAMD12-AS1 caused a reduction in p53 protein levels by shortening its half-life. Conversely, knockdown of SAMD12-AS1 prolonged the half-life of p53. We further demonstrated that SAMD12-AS1 increased the interaction of HDM2 and p53 and enhanced p53 ubiquitination. Our findings reveal that HBV-upregulated SAMD12-AS1 regulates cell proliferation and apoptosis via the NPM1-HDM2-p53 axis.
| S-EPMC6691116 | biostudies-literature
Project description:Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non‑coding RNA (lncRNA) Kinectin 1‑Antisense RNA 1 (KTN1‑AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1‑AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1‑AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1‑AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1‑AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1‑AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA‑505‑3p (miR‑505‑3p) was a promising target of KTN1‑AS1, and the suppressing effects of miR‑505‑3p on cell proliferation and invasive ability was reversed by downregulating KTN1‑AS1. Taken together, the results from the present provided novel insights into the roles of KTN1‑AS1 in GBM, and suggested that the KTN1‑AS1/miR‑505‑3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM.
| S-EPMC7640367 | biostudies-literature
Project description:PurposeLong noncoding RNAs (lncRNA) play critical roles in cancer development. In this study, we aimed to explore the function and possible molecular mechanism of HMMR-AS1 involved in lung adenocarcinoma (LUAD).Experimental designFirstly, we analyzed HMMR-AS1 expression in LUAD tissues with the sequencing data from The Cancer Genome Atlas (TCGA). Next, we evaluated the effects of HMMR-AS1 on LUAD cell proliferation and apoptosis, and its regulation of miR-138 by acting as a ceRNA. The animal model was used to support the in vitro experimental findings.ResultsHMMR-AS1 expression was significantly upregulated in LUAD tissues and was associated with larger tumor diameter, advanced TNM stage, lymph node metastasis, and shorter survival. Knockdown of HMMR-AS1 induced apoptosis and growth arrest in vitro and inhibited tumorigenesis in mouse xenografts. Mechanistically, HMMR-AS1 functioned as a ceRNA of miR-138, thereby leading to repression of its endogenous target sirt6. Moreover, knockdown of HMMR-AS1 dramatically inhibited tumor growth and metastasis of LUAD in vivo.ConclusionsTaken together, HMMR-AS1 is significantly over-expressed in LUAD, and HMMR-AS1-miR-138-sirt6 axis play a critical role in LUAD tumorigenesis. Our findings highlight an oncogenic role of HMMR-AS1 in LUAD.
| S-EPMC6555459 | biostudies-literature
Project description:Transcription factor TFEB is thought to control cellular functions - including in the vascular bed - primarily via regulation of lysosomal biogenesis and autophagic flux. Here, we report that TFEB also orchestrates a non-canonical program that controls the cell-cycle/VEGFR2 pathway in the developing vasculature. In endothelial cells, TFEB depletion halts proliferation at the G1-S transition by inhibiting the CDK4/Rb pathway. TFEB-deficient cells attempt to compensate for this limitation by increasing VEGFR2 levels at the plasma membrane via microRNA-mediated mechanisms and controlled membrane trafficking. TFEB stimulates expression of the miR-15a/16-1 cluster, which limits VEGFR2 transcript stability and negatively modulates expression of MYO1C, a regulator of VEGFR2 trafficking to the cell surface. Altered levels of miR-15a/16-1 and MYO1C in TFEB-depleted cells cause increased expression of plasma-membrane VEGFR2, but in a manner associated with low signaling strength. An endothelium-specific Tfeb knockout mouse model displays defects in fetal and newborn mouse vasculature caused by reduced endothelial proliferation and by anomalous function of the VEGFR2 pathway. These previously unrecognized functions of TFEB expands its role beyond regulation of the autophagic pathway in the vascular system.
| S-SCDT-EMBOJ-2017-98250 | biostudies-other
Project description:Transcription factor TFEB is thought to control cellular functions-including in the vascular bed-primarily via regulation of lysosomal biogenesis and autophagic flux. Here, we report that TFEB also orchestrates a non-canonical program that controls the cell cycle/VEGFR2 pathway in the developing vasculature. In endothelial cells, TFEB depletion halts proliferation at the G1-S transition by inhibiting the CDK4/Rb pathway. TFEB-deficient cells attempt to compensate for this limitation by increasing VEGFR2 levels at the plasma membrane via microRNA-mediated mechanisms and controlled membrane trafficking. TFEB stimulates expression of the miR-15a/16-1 cluster, which limits VEGFR2 transcript stability and negatively modulates expression of MYO1C, a regulator of VEGFR2 trafficking to the cell surface. Altered levels of miR-15a/16-1 and MYO1C in TFEB-depleted cells cause increased expression of plasma membrane VEGFR2, but in a manner associated with low signaling strength. An endothelium-specific Tfeb-knockout mouse model displays defects in fetal and newborn mouse vasculature caused by reduced endothelial proliferation and by anomalous function of the VEGFR2 pathway. These previously unrecognized functions of TFEB expand its role beyond regulation of the autophagic pathway in the vascular system.
| S-EPMC6356157 | biostudies-literature