Ontology highlight
ABSTRACT:
PROVIDER: PRJNA481759 | ENA |
REPOSITORIES: ENA
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Project description:LncRNA MACC1-AS1 is the antisense RNA of MACC1 mRNA, which is located on the sixth intronic of MACC1 gene. MACC1-AS1 is an oncogenic lncRNA in colorectal cancer. But the function role of MACC1-AS1 in breast cancer is unknown. In the present study, We used MS2-Tagged RNA Affinity Purification and miRNA-Seq to characterize microRNAs that associated with MACC1-AS1 in breast cancer cell line MDA231.
2019-04-17 | GSE129873 | GEO
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
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 | GSE97049 | GEO
Project description:Lung metastasis is a major factor affecting long-term survival in adenoid cystic carcinoma patients. Here, we report the long noncoding RNA (lncRNA) MRPL23 antisense RNA 1 (MRPL23-AS1), which exhibited remarkably upregulated expression and was correlated with lung metastasis and overall survival in salivary adenoid cystic carcinoma (SACC) patients. To further study which biological process MRPL23-AS1 may be involved in, SACC-83 cells treated with the control vector or MRPL23-AS1-overexpressing vector were subjected to an mRNA microarray. GO analysis was used to identify the significant biological functions of differentially expressed mRNAs.
2019-08-31 | GSE136697 | GEO
Project description:We identified ADIRF-AS1 as a BMAL1-CLOCK regulated circadian lncRNA. Loss of ADIRF-AS1 in U2OS cells altered rhythmicity of clock-controlled genes and expression of genes associated with cell adhesion and the extracellular matrix (ECM) but did not affect neighboring genes in cis. Affinity based enrichment of U2OS ADIRF-AS1-interacting proteins identified all components of the tumor suppressive PBAF (PBRM1/BRG1) complex. Because PBRM1 is a tumor suppressor mutated in 40% of clear cell renal carcinoma (ccRCC) cases, we studied ccRCC 786O cells and also found PBRM1 bound to ADIRF-AS1. Reducing ADIRF-AS1 expression in 786O and A498 ccRCC cells decreased expression of PBAF-suppressed genes, consistent with ADIRF-AS1 acting to antagonize the function of PBAF. Loss of PBRM1, however, rescued PBAF responsive cell cycle genes in ADIRF-AS1 KO 786O ccRCC cells. Importantly, ADIRF-AS1 expression correlates with survival in human ccRCC, particularly in PBRM1 wild-type, but not mutant PBRM1 tumors. In this regard, loss of ADIRF-AS1 did not affect in vitro 786O cell growth, but strikingly eliminated in vivo tumorigenesis, which was partially rescued by concurrent loss of PBRM1. This rescue, however, requires Matrigel, suggesting a PBRM1-independent function of ADIRF-AS1 in regulating the ECM. Collectively, our findings suggest that ADIRF-AS1 functions partly to antagonize the tumor suppressive effect of the PBAF complex and behaves as an unforeseen BMAL1-regulated, oncogenic lncRNA.
| MSV000090286 | MassIVE
Project description:We identified that SLC25A25-AS1 was a lncRNA influencing radiation response. Therefore, we aimed to explore more biological roles of SLC25A25-AS1 in this process. Towards this end, we used RNA interference (RNAi)-mediated knockdown of SLC25A25-AS1 in HT29 and SW480 to explore the changes of mRNA expression profiles and explore the phenotype outcomes.
2017-03-03 | GSE95605 | GEO
Project description:ZBP1/IMP1 is a RNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. To determine important LncRNA for breast tumor growth and metastasis in response to IMP1 expression, LncRNA expression data were obtained from, and compared between the breast cancer cell line MDA231-IMP1 and MDA231/GFP.
2016-12-09 | GSE91057 | GEO
Project description:Purpose: To identify downstream signaling pathways that mediate functions of GALNT14 Methods: RNAs isolated from MDA231-LM2 cells expressing shCntr or shGALNT14 and MDA231-Par cells expressing pBabe-Hygro control vector or GALNT14 expression vector were analyzed by using an Illumina HiSeq 2500 Conclusions: Our study represents the first transcriptome profile of GALNT14-depleted MDA231-LM2 and GALNT14-overexpressing Par cells.
2019-08-22 | GSE72111 | GEO
Project description:Long noncoding RNAs (lncRNAs) regulate gene expression via their RNA product or through transcriptional interference, yet a strategy to differentiate these two processes is missing. We employed siRNAs to specifically target GNG12-AS1, a lncRNA overlapping the tumour suppressor DIRAS3, transcriptionally or post-transcriptionally. lncRNA transcriptional silencing by siRNA was mediated by Argounate 2 and led to the upregulation of DIRAS3 transcription through switch in RNA polymerase II binding and active histone marks. Conversely, post-transcriptional silencing of GNG12-AS1 had no effect on DIRAS3 expression. Thus, our findings reveal how RNAi machinery can be used to decouple the process and products of lncRNA transcription. The goal of this study was to identify genes regulated by long noncoding RNA GNG12-AS1 in human cells RNA was extracted from human cells (HB2, SUM159) treated with control and GNG12-AS1 siRNAs. The analysis was performed with six biological replicates for each cell line.
2015-11-12 | E-GEOD-60561 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) regulate gene expression via their RNA product or through transcriptional interference, yet a strategy to differentiate these two processes is missing. We employed siRNAs to specifically target GNG12-AS1, a lncRNA overlapping the tumour suppressor DIRAS3, transcriptionally or post-transcriptionally. lncRNA transcriptional silencing by siRNA was mediated by Argounate 2 and led to the upregulation of DIRAS3 transcription through switch in RNA polymerase II binding and active histone marks. Conversely, post-transcriptional silencing of GNG12-AS1 had no effect on DIRAS3 expression. Thus, our findings reveal how RNAi machinery can be used to decouple the process and products of lncRNA transcription. The goal of this study was to identify genes regulated by long noncoding RNA GNG12-AS1 in human cells RNA was extracted from human cells (HB2, SUM159) treated with control and GNG12-AS1 siRNAs. The analysis was performed with six biological replicates for each cell line.
2015-11-12 | E-GEOD-60562 | biostudies-arrayexpress