High-throughput microRNA profile in adult and pediatric primary glioblastomas: the role of miR-10b-5p and miR-630 in the tumor aggressiveness

2020 ◽  
Vol 47 (9) ◽  
pp. 6949-6959
Author(s):  
Luiz Guilherme Darrigo Junior ◽  
Mirella Baroni ◽  
Régia Caroline Peixoto Lira ◽  
Silvia Teixeira ◽  
Paola Fernanda Fedatto ◽  
...  
Keyword(s):  
High Throughput ◽  
Tumor Aggressiveness ◽  
Microrna Profile ◽  
Primary Glioblastomas

scholarly journals O-GlcNAcylation protein disruption by Thiamet G promotes changes on the GBM U87-MG cells secretome molecular signature

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Maria Cecilia Oliveira-Nunes ◽  
Glaucia Julião ◽  
Aline Menezes ◽  
Fernanda Mariath ◽  
John A. Hanover ◽  
...  
Keyword(s):  
Experimental Evidence ◽  
Critical Role ◽  
Molecular Signature ◽  
Label Free ◽  
Intercellular Signaling ◽  
Tumor Aggressiveness ◽  
Signaling Axis ◽  
Literature Evidence ◽  
Therapeutic Tools

AbstractGlioblastoma (GBM) is a grade IV glioma highly aggressive and refractory to the therapeutic approaches currently in use. O-GlcNAcylation plays a key role for tumor aggressiveness and progression in different types of cancer; however, experimental evidence of its involvement in GBM are still lacking. Here, we show that O-GlcNAcylation plays a critical role in maintaining the composition of the GBM secretome, whereas inhibition of OGA activity disrupts the intercellular signaling via microvesicles. Using a label-free quantitative proteomics methodology, we identified 51 proteins in the GBM secretome whose abundance was significantly altered by activity inhibition of O-GlcNAcase (iOGA). Among these proteins, we observed that proteins related to proteasome activity and to regulation of immune response in the tumor microenvironment were consistently downregulated in GBM cells upon iOGA. While the proteins IGFBP3, IL-6 and HSPA5 were downregulated in GBM iOGA cells, the protein SQSTM1/p62 was exclusively found in GBM cells under iOGA. These findings were in line with literature evidence on the role of p62/IL-6 signaling axis in suppressing tumor aggressiveness and our experimental evidence showing a decrease in radioresistance potential of these cells. Taken together, our findings provide evidence that OGA activity may regulate the p62 and IL-6 abundance in the GBM secretome. We propose that the assessment of tumor status from the main proteins present in its secretome may contribute to the advancement of diagnostic, prognostic and even therapeutic tools to approach this relevant malignancy.

scholarly journals Fast and Efficient 5′P Degradome Library Preparation for Analysis of Co-Translational Decay in Arabidopsis

Plants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 466
Author(s):  
Marie-Christine Carpentier ◽  
Cécile Bousquet-Antonelli ◽  
Rémy Merret
Keyword(s):  
Gene Expression ◽  
Quality Control ◽  
Transcriptional Regulation ◽  
High Throughput ◽  
Library Preparation ◽  
Working Day ◽  
Set Up ◽  
Post Transcriptional Regulation ◽  
Commercial Kit

The recent development of high-throughput technologies based on RNA sequencing has allowed a better description of the role of post-transcriptional regulation in gene expression. In particular, the development of degradome approaches based on the capture of 5′monophosphate decay intermediates allows the discovery of a new decay pathway called co-translational mRNA decay. Thanks to these approaches, ribosome dynamics could now be revealed by analysis of 5′P reads accumulation. However, library preparation could be difficult to set-up for non-specialists. Here, we present a fast and efficient 5′P degradome library preparation for Arabidopsis samples. Our protocol was designed without commercial kit and gel purification and can be easily done in one working day. We demonstrated the robustness and the reproducibility of our protocol. Finally, we present the bioinformatic reads-outs necessary to assess library quality control.

scholarly journals The role of high-throughput transcriptome analysis in metabolic engineering

2005 ◽  
Vol 10 (5) ◽  
pp. 385-399 ◽  
Author(s):  
Michael C. Jewett ◽  
Ana Paula Oliveira ◽  
Kiran Raosaheb Patil ◽  
Jens Nielsen
Keyword(s):  
Metabolic Engineering ◽  
High Throughput ◽  
Transcriptome Analysis

scholarly journals Applications of Metabolomics in Forensic Toxicology and Forensic Medicine

2021 ◽  
Vol 22 (6) ◽  
pp. 3010
Author(s):  
Michal Szeremeta ◽  
Karolina Pietrowska ◽  
Anna Niemcunowicz-Janica ◽  
Adam Kretowski ◽  
Michal Ciborowski
Keyword(s):  
Machine Learning ◽  
Multivariate Statistics ◽  
High Throughput ◽  
Forensic Medicine ◽  
Forensic Toxicology ◽  
Metabolic Changes ◽  
Untargeted Metabolomics ◽  
Criminal Cases ◽  
Statistical Approaches

Forensic toxicology and forensic medicine are unique among all other medical fields because of their essential legal impact, especially in civil and criminal cases. New high-throughput technologies, borrowed from chemistry and physics, have proven that metabolomics, the youngest of the “omics sciences”, could be one of the most powerful tools for monitoring changes in forensic disciplines. Metabolomics is a particular method that allows for the measurement of metabolic changes in a multicellular system using two different approaches: targeted and untargeted. Targeted studies are focused on a known number of defined metabolites. Untargeted metabolomics aims to capture all metabolites present in a sample. Different statistical approaches (e.g., uni- or multivariate statistics, machine learning) can be applied to extract useful and important information in both cases. This review aims to describe the role of metabolomics in forensic toxicology and in forensic medicine.

The Role of Epigenetics in Cancer: From Molecular Function to High-Throughput Assays

2011 ◽  
pp. 137-152
Author(s):  
Aleksandra Pekowska ◽  
Joaquin Zacarias-Cabeza ◽  
Jinsong Jia ◽  
Pierre Ferrier ◽  
Salvatore Spicuglia
Keyword(s):  
High Throughput ◽  
Molecular Function

CTNND1 to mediate bone metastasis of triple-negative breast cancer via regulating CXCR4.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e13045-e13045
Author(s):  
Chang Gong ◽  
Qun Lin ◽  
Xiaolin Fang ◽  
Wenguo Jiang ◽  
Jun Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bone Metastasis ◽  
High Throughput ◽  
Triple Negative Breast Cancer ◽  
High Throughput Sequencing ◽  
Triple Negative ◽  
Mtor Pathway ◽  
Tissue Samples

e13045 Background: Compared to lumial breast cancer, the proporation of triple-negative breast cancer (TNBC) with bone metastases (BMs) is relatively low and few data focusing on the mechanism of the BMs in TNBC are available, Here, we screened that CTNND1 was associated with BMs of TNBC by integrating high-throughput sequencing, and further investigated the role of CTNND1 in BMs of TNBC in vitro. Methods: TNBC tissue samples with only BMs (n = 6) and without any metastasis (n = 10) were tested using high-throughput sequencing and 11 differentially expressed relative genes were identified. We then quantified these 11 genes in normal breast tissue samples (n = 26), TNBC tissue samples with only BMs (n = 10), TNBC tissue samples without any metastasis (n = 88) as well as luminal tissue samples with BMs（n = 10）through qPCR and immunohistochemical staining (IHC). The effects of knocking down CTNND1 on the interaction between TNBC cells and osteoblasts were examined by cell adhesion, transwell migration and matrigel invasion assays. To explorethe role of CTNND1 in mediating bone metastasis in TNBC, we used RNA-sequencing to find out the relative downstream gene CXCR4 and PI3K-AKT-mTOR pathway and verified it in vitro by Western Blotting. Results: Combining our high-throughput sequencing data, qPCR and IHC in clinical tissue samples, we verified that CTNND1 was decreased in TNBC patients with bone metastasis compared to normal tissue and luminal tissue with BMs. Knocking down of CTNND1 in TNBC cells including MDA-MB-231, MDA-MB-468 and BT549 weakened cells adhesion, but facilitated cells migration and invasion. Mechanically, knocking down of CTNND1 upregulated CXCR4 via activating PI3K-AKT-mTOR pathway in TNBC but not luminal and HER2- positive breast cancer cells lines. Conclusions: CTNND1 mediates bone metastasis in triple-negative breast cancer via regulating CXCR4.CTNND1 may serve as a potential predictor of bone metastasis for TNBC patients.

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