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.
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.
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).
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.
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.
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.
Project description:Our data showed that ELF3-AS1 was a nuclear lncRNA, and its biofunction in cancers is largely unknown to date. To explore the function of lncRNA ELF3-AS1 in gastric cancer, loss-of-function study was performed in SGC7901 and AGS cell lines. RNA sequencing studies showed that the expression of almost all the histone coding genes were significantly increased after knocking down of ELF3-AS1 in SGC7901 and AGS cell lines.
Project description:Background: The lack of obvious symptoms of early gastric cancer (GC) as well as the absence of sensitive and specific biomarkers results in poor clinical outcomes. Tubulin is currently emerging as important regulators of the microtubule cytoskeleton and thus have a strong potential to be implicated in a number of disorders, however, its mechanism of action in gastric cancer is still unclear. Tubulin alpha-1C(TUBA1C) is a subtype of α-tubulin, high TUBA1C expression has been shown to be closely related to a poor prognosis in in various cancers,this study, for the first time, revealed the mechanism of TUBA1C promotes malignant progression of gastric cancer in vitro and in vivo. Methods: The expression of lncRNA EGFR-AS1 was detected in human GC cell lines by qRT–PCR. Mass spectrometry experiments following RNA pulldown assays found that EGFR-AS1 directly binds to TUBA1C, the CCK8, EdU, transwell, wound-healing, cell cycle assays and animal experiments were conducted to investigate the function of TUBA1C in GC. Combined with bioinformatics analyses, reveal interaction between Ki-67, E2F1, PCNA and TUBA1C by western blot. Rescue experiments furtherly demonstrated the relationship of EGFR-AS1and TUBA1C. Results: TUBA1C was proved to be a direct target of EGFR-AS1, TUBA1C promotes gastric cancer proliferation, migration and invasion by accelerating the progression of the cell cycle from the G1 phase to the S phase and activating the expression of oncogenes: Ki-67,E2F1 and PCNA. Conclusions: TUBA1C is a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression and could be a novel biomarker and therapeutic target for GC.