Development of gene expression signatures for lncRNA MRPL23-AS1
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ABSTRACT:
PROVIDER: PRJNA563063 | ENA |
REPOSITORIES: ENA
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Project description:Development of gene expression signatures for lncRNA MRPL23-AS1 up-regulation
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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.
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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-LM cells treated with si-control or si-MRPL23-AS1 were subjected to an mRNA microarray. GO analysis was used to identify the significant biological functions of differentially expressed mRNAs.
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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).
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Project description:Long non-coding RNAs (lncRNAs) comprise a diverse class of gene expression regulators with emerging roles in many biological processes including cancer. Here we show that the expression of the lncRNA Hedgehog Interacting Protein Antisense 1 (HHIP-AS1) is a hallmark feature of human SHH-driven tumors. Importantly, loss of HHIP-AS1 leads to reduced tumor growth in SHH-driven tumors in vitro and in vivo. Our results demonstrate the power of cross-entity transcriptome-wide comparisons to identify novel epigenetic–regulatory lncRNA circuitries underlying human cancers.
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Project description:M2-like macrophage upregulated lncRNA ADPGK-AS1 regulates macrophage phenotype and modulates the influence of macrophages on lung tumor apoptosis and migration. Here we identified proteins that interact with ADPGK-AS1 that might give insight into how this regulation this is regulated on molecular level. We were able to identify interaction with mitochondrial ribosomal proteins, leading to regulation of mitochondrial oxidative phosphorylation.
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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.
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