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LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression [miRNA-Seq]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE178397 | GEO | 2024/06/17

REPOSITORIES: GEO

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LncRNA HIF1A-AS1 regulates the apoptosis and proliferation of vascular endothelial cells through globally regulating miRNAs expression [RNA-Seq]

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

Transcriptomics provides novel insights into the regulatory mechanism of lncRNA HIF1A-AS1 on VSMCs

Project description:In current study, using a lentivirus-based expression system, we observed that overexpressing HIF1A-AS1 successfully promoted apoptosis, significantly altered cell cycle distribution and greatly facilitated migration in VSMCs, further highlighting the robust promoting effects of HIF1A-AS1 to TAA. Moreover, transcriptomics was implemented to uncover its underlying mechanism. A total of 175 differentially expressed genes (DEGs) were identified, with some of them enriched in apoptosis, migration and cell cycle related pathways. Intriguingly, some DEGs were annotated in vascular development or coagulation function pathways. In view of this, we suggested HIF1A-AS1 mediated the progression of TAA by not only regulating the function of VSMC cells, but also altering vascular development or coagulation function. Lastly, RT-qPCR confirmed the veracity and reliability of RNA-sequencing results.

2023-10-12 | GSE202078 | GEO

MAGE-A1 Promotes Proliferation, Migration and Invasion of Human Melanoma Cells through RNA-SEQ Analysis via Affecting C-JUN-IL8-ARHGAP29 Network

Project description:To define the role of MAGE-A1 in melanoma growth and metastasis, we performed RNA-seq analysis on MAGE-A1 overexpression (OE) and knockdown (KD) models in A375 human melanoma cell line. Our results revealed that overexpression of MAGE-A1 dramatically promoted proliferation, migration, and invasion of human melanoma cells in vitro and down-regulated of MAGE-A1 inhibited tumor cell proliferation and invasion. Furthermore, MAGE-A1 exerts its tumor promoting activity via activating including ERK-MAPK signaling pathway by RNA-seq analysis. mRNA profiles of MAGE-A1 over expression (OE), knockdown (KD), pcDNA-vector control, and pRNAT-scramble control in A375 cell line were generated using Ion torrent

2016-01-04 | E-GEOD-66859 | biostudies-arrayexpress

A Long Noncoding RNA TTN-AS1 Controls Esophageal Squamous Cell Carcinomas by Functioning as a Competing Endogenous RNA and Scaffolding mRNA Stabilizing Protein HuR [Agilent]

Project description:BACKGROUND & AIMS: Emerging long non-coding RNAs (lncRNAs) have been demonstrated to be associated with progression of various cancers. In the current study, we identified a novel lncRNA-TTN-AS1 and dissected the underlying mechanisms by which lncRNA-TTN-AS1 induced carcinogenesis of esophageal squamous cell carcinoma (ESCC). METHODS: ESCC and adjacent non-malignant specimens from 7 ESCC patients were chosen to analyze the expression profiles of lncRNA-miRNA-mRNA using multiple microarrays. The novel lncRNA-TTN-AS1 was identified using multiple bioinformatics platforms. Levels of lncRNA-TTN-AS1 in tissues from 148 ESCC patients were verified by qRT-PCR and in situ hybridization. The biological function and mechanism of action of lncRNA-TTN-AS1 were performed both in vivo and in vitro using gain-of and loss-of function assays on TE-13 cells and KYSE-410 cells, luciferase reporter assays, RNA immunoprecipitation (RIP) assays and RNA pull-down assays. RESULTS: lncRNA-TTN-AS1 levels were upregulated in ESCC tissues compared with adjacent non-malignant tissues, and correlated with poor prognosis. LncRNA-TTN-AS1, as an oncogene, promoted ESCC cell proliferation and prevented apoptosis. Additionally, lncRNA-TTN-AS1 increased snail1 levels by competitively binding to miR-133b, thereby facilitating epithelial-mesenchymal transition (EMT) cascades. Sharing miR-133b binding sites, lncRNA-TTN-AS1 as a ceRNA also derepressed FSCN1 mediated by miR-133b. Notably, lncRNA-TTN-AS1 stabilized FSCN1 mRNA by interacting directly with the mRNA stabilizing protein HuR, resulting in ESCC invasion-cascades and activation of FSCN1/β-catenin. CONCLUSION: lncRNA-TTN-AS1 sponges miR-133b to govern the expression of snial1 and FSCN1, which promotes ESCC cell proliferation and metastasis. It also combines with HuR to modulate FSCN1 in ESCC cell lines. Our findings may provide a novel target for ESCC anti-metastatic therapies.

2017-03-28 | GSE97050 | GEO

A Long Noncoding RNA TTN-AS1 Controls Esophageal Squamous Cell Carcinomas by Functioning as a Competing Endogenous RNA and Scaffolding mRNA Stabilizing Protein HuR [Affymetrix]

2017-03-28 | GSE97049 | GEO

MAGE-A1 Promotes Proliferation, Migration and Invasion of Human Melanoma Cells through RNA-SEQ Analysis via Affecting C-JUN-IL8-ARHGAP29 Network

2016-01-04 | GSE66859 | GEO

Deciphering the molecular mechanism of long non-coding RNA HIFA-AS1 regulating pancreatic cancer cells

Project description:HIFA-AS1, an antisense transcript of HIF1α gene, is a 652-bp long non-coding RNA (lncRNA) which globally expressed in multiple tissues of animals. Recent evidence indicated that the HIFA-AS1 was involved in tumorigenesis of several types of cancer, but there were no reports on pancreatic cancer (PC). In order to investigate whether the HIFA-AS1 could mediate the PC or not, it was overexpressed in a PC cell line (PANC-1), and a series of experiments including cell viability detection, flow cytometry, and transwell migration were performed. Functionally, the results indicated that overexpression (OE) of HIFA-AS1 could inhibit proliferation and shift, and promote apoptosis of PC cells. Moreover, to explore underlying molecular mechanism of HIFA-AS1 in PC cells, the iTRAQ (isobaric tags for relative and absolute quantification) quantitative proteomics analysis was implemented. Mechanistically, it was found that OE of HIFA-AS1 globally affected the expression levels of multiple protein associated with metabolism of cancer, suggesting that HIFA-AS1 might regulate the tumorigenesis of PC by up- and down-regulating the gene expression.

2021-09-23 | PXD028727 | iProX

Identification of interacting proteins of lncRNA HIF1α-AS1

Project description:LncRNA Hypoxia-inducible factor 1α-antisense 1 (HIF1α-AS1) is located on the antisense strand of the important Hypoxia-inducible factor 1α (HIF1α) gene, but being transcribed in antisense direction along the HIF1α promoter. Here we used the 3’end biotinylated HIF1a-AS1 RNA and a control RNA for RNA Pulldown and searched for interacting proteins in nuclear extracts of human umbilical vein endothelial cells (HUVEC).

2022-09-23 | PXD023512 | Pride

Effect of ZFPM2-AS1 knockdown on gene expression of breast malignant phyllode tumor cells.

Project description:ZFPM2-AS1 can promote the proliferation, migration and invasion of tumor cells, but its mechanism is still unclear.To investigate the molecular mechanism of malignant progression of breast phyllode tumors, we knocked down the expression of ZFPM2-AS1 in malignant phyllode tumor cells, and detected the genes regulated by ZFPM2-AS1 by RNAseq.

2024-06-20 | GSE235268 | GEO

Microarray profiling analysis of circular RNAs expression in bladder cancer [lncRNA profiling]

Project description:Background: Growing evidence has shown the association of long noncoding RNA/microRNA/mRNA is implicated in tumor initiation, development, and progression. Long noncoding RNA (lncRNA) HAND2-AS1 exhibits anti-cancer effects in diverse cancers. However, the knowledge of HAND-AS1 in bladder cancer remains largely unknown. The present study aims to investigate the effects and mechanisms of HAND-AS1 in bladder cancer progression. Methods: The expression of lncRNA was analyzed by RT2 lncRNA PCR Arrays. The differential expressed lncRNAs were further verified by qRT-PCR. The relationship between lncRNA expression and clinical features was evaluated with Spearman correlation test. Cell proliferation was measured by MTT assay. Cell apoptosis percentage was detected by ANNEXIN V-PI analysis. The promoter activity was illustrated by Luciferase assay, and the change of microRNA and protein was detected by qRT-PCR and western blot, separately. Results: The expression of HAND2-AS1 declined in bladder cancer and correlated with depth of invasion and grades negatively. Restoration of HAND2-AS1 hampered cell growth by provoking cell apoptosis. Furthermore, one of the HAND2-AS1 sponge, miR-146, was found overexpression in bladder cancer tissue and cell lines. Expression of miR-146 related to HAND2-AS1 expression negatively. One of the targeted genes of miR-146, retinoic acid receptor beta (RARB) was downregulated in bladder cancer. In addition, the expression of RARB related to miR-146 negatively. Lost-of-function and gain-of-function experiments were used to identify the mechanisms underlying association of lncRNA HAND2-AS1: miR-146: RARB. miR-146 targeted RARB directly and hindered RARB-mediate apoptosis. However, the hindrance was impaired by HAND2-AS1 notably. Conclusion: HAND2-AS1 diminished miR-146 expression, thereby releasing the suppression of miR-146 on RARB-mediated apoptosis, promoting bladder cancer regression.

2020-11-18 | GSE140585 | GEO

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