Dataset Information

FA-SAT ncRNA interactome

ABSTRACT: FA-SAT is a satellite DNA sequence present and transcribed in many Bilateria species, what may anticipate a conserved and significant function in these genomes. Here we prove that in cat and human cells, FA-SAT satellite transcripts play a nuclear function at the G1 phase of the cell cycle. We identified and demonstrated that the main FA-SAT non-coding RNA interactor is the PKM2 protein. Our work shows that the disruption of the FA-SAT ncRNA/PKM2 protein complex, by the depletion of either FA-SAT or PKM2, results in the same phenotype—apoptosis. Moreover, the ectopic overexpression of FA-SAT in tumour human cells did not affect the cell cycle progression. In sum, our data reveal a new player, FA-SAT RNA, a non-coding satellite RNA, which interacts with the PKM2 nuclear protein. This ribonucleoprotein is involved in apoptosis and cell cycle progression, what foresees a promising new target for studies in cancer processes that rely on these pathways.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human) Bos Taurus (bovine) Felis Silvestris

SUBMITTER: Sandra Anjo

LAB HEAD: Bruno Manadas

PROVIDER: PXD010081 | Pride | 2020-03-19

REPOSITORIES: Pride

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Publications

FA-SAT ncRNA interacts with PKM2 protein: depletion of this complex induces a switch from cell proliferation to apoptosis.

Ferreira Daniela D Escudeiro Ana A Adega Filomena F Anjo Sandra I SI Manadas Bruno B Chaves Raquel R

Cellular and molecular life sciences : CMLS 20190725 7

FA-SAT is a highly conserved satellite DNA sequence transcribed in many Bilateria species. To disclose the cellular and functional profile of FA-SAT non-coding RNAs, a comprehensive experimental approach, including the transcripts location in the cell and in the cell cycle, the identification of its putative protein interactors, and silencing/ectopic expression phenotype analysis, was performed. FA-SAT non-coding RNAs play a nuclear function at the G1 phase of the cell cycle and the interactomic ...[more]

PMID: 31346634

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Project description:Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

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Dataset Information

FA-SAT ncRNA interactome

Publications

FA-SAT ncRNA interacts with PKM2 protein: depletion of this complex induces a switch from cell proliferation to apoptosis.

Similar Datasets

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