Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CircRNA expression data from human non-small cell lung cancer tissues and the correponding non-cancerous tissues

ABSTRACT: Circular RNAs (circRNAs) are a class of covalently closed single-stranded RNAs that have been demonstrated to involve in cancer progression. Here, we identify circNDUFB2 is downregulated in non-small cell lung cancer (NSCLC) tissues, and it negatively correlates with the malignant features. Elevated circNDUFB2 inhibits growth and metastasis of NSCLC cells. circNDUFB2 functions as a scaffold to enhance interaction of TRIM25 with IGF2BPs by forming a TRIM25/circNDUFB2/IGF2BPs ternary complex. The resultant ternary complex facilitates ubiquitination degradation of IGF2BPs, and N6-methyladenosine (m6A) modification of circNDUFB2 increases ubiquitination efficiency of TRIM25 for IGF2BPs. Moreover, circNDUFB2 can be recognized by RIG-I, then activates RIG-I-MAVS signaling cascades and recruits immune cells into tumor microenvironment (TME). Our data provide evidences that circNDUFB2 participates in degradation of IGF2BPs and activation of anti-tumor immunity in NSCLC progression. These findings reveal a dual-role pattern of circNDUFB2 action involved in protein ubiquitination degradation and cellular immune response.

ORGANISM(S): Homo sapiens

PROVIDER: GSE158695 | GEO | 2020/10/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor immunity

Project description:Circular RNAs (circRNAs) are a class of covalently closed single-stranded RNAs that have been demonstrated to involve in cancer progression. Here, we identify circNDUFB2 is downregulated in non-small cell lung cancer (NSCLC) tissues, and it negatively correlates with the malignant features. Elevated circNDUFB2 inhibits growth and metastasis of NSCLC cells. circNDUFB2 functions as a scaffold to enhance interaction of TRIM25 with IGF2BPs by forming a TRIM25/circNDUFB2/IGF2BPs ternary complex. The resultant ternary complex facilitates ubiquitination degradation of IGF2BPs, and N6-methyladenosine (m6A) modification of circNDUFB2 increases ubiquitination efficiency of TRIM25 for IGF2BPs. Moreover, circNDUFB2 can be recognized by RIG-I, then activates RIG-I-MAVS signaling cascades and recruits immune cells into tumor microenvironment (TME). Our data provide evidences that circNDUFB2 participates in degradation of IGF2BPs and activation of anti-tumor immunity in NSCLC progression. These findings reveal a dual-role pattern of circNDUFB2 action involved in protein ubiquitination degradation and cellular immune response.

2020-08-22 | GSE156607 | GEO

TRIM25 promotes glioblastoma cell growth and invasion via regulation of the PRMT1/c-MYC pathway by targeting the splicing factor NONO

Project description:Ubiquitination plays an important role in proliferating and invasive characteristic of glioblastoma (GBM), similar to many other cancers. Tripartite motif 25 (TRIM25) is a member of the TRIM family of proteins, which are involved in tumorigenesis through substrate ubiquitination. Here, we found TRIM25 is upregulated in GBM and promotes glioblastoma cell growth and invasion, both in vitro and in vivo. Subsequently, we screened a panel of proteins that interact with TRIM25; mass spectrometry and co-immunoprecipitation showed that NONO was a potential substrate of TRIM25. TRIM25 knockdown reduced the K63-linked ubiquitination of NONO, which suppressed the splicing function of NONO. The dysfunctional NONO further leads to the retention of the second intron in the pre-mRNA of PRMT1 and inhibit the activation of the PRMT1/c-MYC pathway. In summary, we demonstrated that TRIM25 promotes glioblastoma cell growth and invasion by regulating the PRMT1/c-MYC pathway through mediation of the splicing factor NONO. Efforts to target the E3 ligase activity of TRIM25 or the complex interactions between TRIM25 and NONO may be useful in the treatment of GBM.

2023-07-11 | GSE236661 | GEO

Ubiquitination of DEAD-box RNA helicase DDX3X by TRIM25

Project description:Tripartite motif protein 25 (TRIM25) is an E3 ligase that ubiquitinates multiple substrates within the RLR signalling cascade and plays both RING (really interesting new gene)-dependent and RING-independent roles in RIG-I-mediated IFN induction. We report that the PRY-SPRY domain of TRIM25 interacts with the N-terminal extension (NTE) of DEAD-box helicase 3X (DDX3X), a host protein with multiple roles in RLR signalling. Gene reporter assays and knockdown studies reveal DDX3X and TRIM25 cooperate to activate the IFN- promoter following RIG-I activation independent of DDX3X’s catalytic activity. We also show that TRIM25 ubiquitinates DDX3X at several lysine residues in vitro and in cells.

2021-09-08 | PXD028122 | Pride

The long noncoding RNA Lnczc3h7a promotes TRIM25-mediated RIG-I antiviral innate immune response

Project description:In this study, we employed a combination of RIP-seq and iCLIP-seq technologies to identify long non-coding RNA associated with cytoplasmic TRIM25 and RIG-I protein in mouse macrophages cells.

2019-03-12 | GSE112175 | GEO

MicroRNA profiles in five pairs of early gastric cancer tissues and adjacent non-cancerous tissues.

Project description:Approximately half of the world's gastric cancer cases and deaths occur in China. In addition, the incidence and mortality rates of gastric cancer in Gansu province in China are much higher than the average nationwide levels. The present study investigated microRNA (miRNA/miR) profiles in early gastric cancer (EGC) without specific symptoms. miRNA expression levels in five pairs of EGC tissues and adjacent non-cancerous mucosa tissues of patients from Gansu province in China were analyzed using a miRNA microarray. A total of 47 differentially expressed miRNAs (DEMs) were identified. Subsequently, mRNA expression profiles of three pairs of cancer tissues and adjacent non-cancerous tissues from 3 Asian patients with stage I or stage II gastric cancer (stage I/II; American Joint Committee on Cancer classification, Eighth Edition) were obtained from The Cancer Genome Atlas database, and differentially expressed genes (DEGs) were identified. The target genes of DEMs were filtered from the DEGs using the miRDB database and a miRNA-gene network was constructed. The functions of DEMs were evaluated using the tool for annotations of human miRNAs database, and via Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes analysis and Gene Set Enrichment Analysis of the target genes. Finally, survival analyses of DEMs, which were in the miRNA-gene network, was performed. The results suggested that a number of miRNAs, including hsa-let-7a-5p, hsa-miR-27a-3p, hsa-miR-126-5p and hsa-miR-424-5p, may serve critical roles in EGC. The present study could provide a basis for the identification of EGC screening biomarkers. Furthermore, the present study may provide a basis for the exploration of the cause of the high incidence of gastric cancer in Gansu province from the perspective of miRNAs.

| S-EPMC8200934 | biostudies-literature

DNA methylation profile of cancerous and non-cancerous renal tissues

Project description:Renal cell carcinoma (RCC), particularly clear cell RCC (ccRCC), is the most common type of kidney tumors characterized by the highest mortality rate of the genitourinary cancers. Lack of symptoms leads to late detection of the disease using conventional imagining procedures. There is an urgent need for new diagnostic biomarkers with the potential for early detection and prediction of high risk of progression. In the present study, based on microarray profiling of DNA methylation in 11 pairs of ccRCC and noncancerous renal tissues (NRT), the methylation at regulatory regions of six putative ccRCC biomarkers was further analyzed in 123 ccRCC and 45 NRT samples by means of methylation specific PCR (MSP). Thereafter, the quantitative MSP was applied for the methylation analysis in the urine samples of 123 ccRCC patients and 93 asymptomatic controls (ASC). The comparison of ccRCC and NRT samples revealed significant methylation differences in 1319 genes, of which 191 were hypermethylated and 1128 were hypomethylated. DNA methylation of selected genes were validated by means of MSP and significantly higher methylation frequencies for all genes was found in ccRCC tissues compared to NRT (33-60% vs. 0-11%). Methylated status of at least one gene was significantly related with various adverse clinical-pathological parameters of the patients, including larger tumor size, higher tumor pathological stage, grade, intravascular and fat invasion as welll as tumor necrosis. The multivariate Cox regression model revealed the methylation in a panel of selected three genes as independent prognostic biomarker of ccRCC. Moreover, five genes were characterised by higher methylation intensity in the urine samples of ccRCC patients, as compared to ASC, and various combination of these biomarkers revealed moderate-to-high sensitivity and specificity values for the diagnosis of ccRCC.

2021-02-15 | GSE166734 | GEO

Gene expression profile of cancerous and non-cancerous renal tissues

Project description:Clear cell renal cell carcinoma (ccRCC), is the most common subtype of kidney tumors and characterised by the highest mortality rates among the genitourinary cancers. The currently used models for predicting patient outcome, are based on clinicopathological features only, however patients with similar measures can still have divergent outcomes. This study aimed at identification of novel prognostic DNA methylation biomarkers to aid in predicting patient survival. As DNA methylation in the most cases is related to alteration of gene expression, firstly, SurePrint G3 Human GE 8×60K Microarrays were used for gene expression profiling in 4 ccRCC tissues and paired non-cancerous renal tissue (NRT) samples. The DNA methylation status of four down-regulated genes were evaluated in 123 ccRCC and 45 NRT samples by means of methylation specific PCR (MSP). Microarray-based transcriptome comparison of 4 ccRCC and 4 NRT samples identified 3942 genes, that were significantly deregulated (P < 0.050) with absolute fold change (FC) value of ≥2. A half of these genes (N = 1958) were down-regulated and four of such genes with moderate-to-high alteration were selected for the further DNA methylation analysis. DNA hypermethylation of all selected genes were cancer specific (P<0.050) with the frequency in tumour tissues ranging from 18 to 42%. The methylated status of at lest one gene showed significant associations with larger tumor size, higher Fuhrman and WHO/ISUP grades as well as the presence of tumor intravascular invasion and necrosis. Moreover, the methylated status of the panel of tree genes was highly predictive for poorer overall survival and outperformed the prognostic value of tumor stage and tumor necrosis. In conclusion, the three-gene DNA methylation biomarker panel predicts outcome of patients with ccRCC and might be used to improve current prognostic models.

2021-03-14 | GSE168845 | GEO

miRNA expressions in non-cancerous and cancerous human gastric tissues

Project description:We investigated the involvement of microRNAs (miRNAs) in gastric cancers. MiRNA expression was profiled from 40 cancerous and 40 non-cancerous tissues obtained from the National Cancer Centre, Singapore, and Singhealth Tissue Repository, Singapore. We identified 80 differentially expressed miRNAs in tumors compared with normal tissues. Among these miRNAs, we identified hsa-mir-486-5p (mir-486) as a significantly downregulated miRNA in GC. Subsequent functional characterization revealed that mir-486 playing a tumor suppressor role. We also observed frequent genomic deletion of mir-486 in 20-30% of GCs. To our knowledge, mir-486 represents one of the first tumor suppressor miRNAs in GC inactivated through genomic deletion.

2011-08-01 | GSE23739 | GEO

Oxidative stress markers in patient-derived non-cancerous cervical tissues and cells.

Project description:High-risk human papillomaviruses (HPV) are the causative agents of cervical cancer. However, not all infected women develop cervical cancer. Cervical tumorigenesis is characterized by a multifactorial etiology, with oxidative stress (OS) likely playing a major role. In addition to exogenous sources, metabolic processes also contribute to OS. In principle, variability in levels of cervical OS has the potential to influence the likelihood of conversion to cervical cancer. To ask whether such variability indeed existed, we assessed the levels of ROS and the oxidative DNA damage biomarker 8-oxodG in normal non-cancerous cervical tissues and cells obtained from women with uterovaginal pelvic organ prolapse following vaginal hysterectomy. We demonstrated five and ten-fold variability between tissues isolated from the transformation zone (TZ) and ectocervix (EC) of different women, respectively. Despite the greater variability (likely due to differences in tissue composition), the overall pattern of ROS levels in EC tissues mirrored those obtained in their corresponding TZ tissues. Our results also show that the levels of ROS in TZ tissues were always higher than or equal to those found in the respective EC tissues, providing a possible explanation for TZ tissue being the primary target for HPV infection and cervical carcinogenesis. Interestingly, primary keratinocytes isolated and cultured from these cervical specimens also displayed high variability in ROS levels, with some strongly mirroring the levels of ROS observed in their corresponding tissues, while others were less closely associated. Finally, we demonstrated that the levels of DNA damage mirrored the levels of ROS in the cultured primary cells. Understanding the factors and mechanisms that dispose certain individuals to develop cervical cancer has the potential to enable the development of approaches that make the conversion of HPV infection to cancer development even more rare.

| S-EPMC7642372 | biostudies-literature

Substrate trapping approach identifies TRIM25 ubiquitination targets involved in diverse cellular and antiviral processes

Project description:The tripartite motif (TRIM) family of E3 ubiquitin ligases is well known for its roles in antiviral restriction and innate immunity regulation, in addition to many other cellular pathways. In particular, TRIM25-mediated ubiquitination affects both carcinogenesis and antiviral response. While individual substrates have been identified for TRIM25, it remains unclear how it regulates diverse processes. Here we characterized a mutation, R54P, critical for TRIM25 catalytic activity, which we successfully utilized to “trap” substrates. We demonstrated that TRIM25 targets proteins implicated in stress granule formation (G3BP1/2), nonsense-mediated mRNA decay (UPF1), and nucleoside synthesis (NME1). R54P abolishes TRIM25 inhibition of alphaviruses independently of the host interferon response, suggesting that this antiviral effect is a direct consequence of ubiquitination. Consistent with that, we observed diminished antiviral activity upon knockdown of several TRIM25-R54P specific interactors including NME1. Our findings highlight that multiple substrates mediate the cellular and antiviral activities of TRIM25, illustrating the multi-faceted role of this ubiquitination network in diverse biological processes.

2022-08-02 | PXD034024 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data