Dataset Information

The M-phase specific hyperphosphorylation of Staufen2 involved the cyclin-dependent kinase CDK1.

ABSTRACT:

Background

Staufen2 (STAU2) is an RNA-binding protein involved in the post-transcriptional regulation of gene expression. This protein was shown to be required for organ formation and cell differentiation. Although STAU2 functions have been reported in neuronal cells, its role in dividing cells remains deeply uncharacterized. Especially, its regulation during the cell cycle is completely unknown.

Results

In this study, we showed that STAU2 isoforms display a mitosis-specific slow migration pattern on SDS-gels in all tested transformed and untransformed cell lines. Deeper analyses in hTert-RPE1 and HeLa cells further indicated that the slow migration pattern of STAU2 isoforms is due to phosphorylation. Time course studies showed that STAU2 phosphorylation occurs before prometaphase and terminates as cells exit mitosis. Interestingly, STAU2 isoforms were phosphorylated on several amino acid residues in the C-terminal half via the cyclin-dependent kinase 1 (Cdk1), an enzyme known to play crucial roles during mitosis. Introduction of phospho-mimetic or phospho-null mutations in STAU2 did not impair its RNA-binding capacity, its stability, its interaction with protein co-factors or its sub-cellular localization, suggesting that STAU2 phosphorylation in mitosis does not regulate these functions. Similarly, STAU2 phosphorylation is not likely to be crucial for cell cycle progression since expression of phosphorylation mutants in hTert-RPE1 cells did not impair cell proliferation.

Conclusions

Altogether, these results indicate that STAU2 isoforms are phosphorylated during mitosis and that the phosphorylation process involves Cdk1. The meaning of this post-translational modification is still elusive.

SUBMITTER: Beaujois R

PROVIDER: S-EPMC5513041 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Publications

The M-phase specific hyperphosphorylation of Staufen2 involved the cyclin-dependent kinase CDK1.

Beaujois Rémy R Ottoni Elizabeth E Zhang Xin X Gagnon Christina C Hassine Sami S Mollet Stéphanie S Viranaicken Wildriss W DesGroseillers Luc L

BMC cell biology 20170714 1

<h4>Background</h4>Staufen2 (STAU2) is an RNA-binding protein involved in the post-transcriptional regulation of gene expression. This protein was shown to be required for organ formation and cell differentiation. Although STAU2 functions have been reported in neuronal cells, its role in dividing cells remains deeply uncharacterized. Especially, its regulation during the cell cycle is completely unknown.<h4>Results</h4>In this study, we showed that STAU2 isoforms display a mitosis-specific slow ...[more]

PMID: 28705199

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Project description:Simple Summary Cyclin-dependent kinase 1 (CDK1), one of the key regulators of the G2/M checkpoint, is expressed in many cells and plays an important role in cell cycle control. However, CDK1 expression is substantially increased in many tumors of diverse origins and is associated with tumorigenesis. Targeting CDK1 shows promising results for several tumors. However, a systematic and integrative analysis of CDK1 in cancer has not been conducted. The present study aims to use pan-cancer analysis to investigate the relationship, similarities, and differences in genetic and cellular changes associated with CDK1 in various tumors and tumor microenvironments. Our findings elucidate that CDK1 expression increases in more than 20 human tumors and is highly correlated with oncogenic signature gene sets, biological pathways, immune cell infiltration, tumor mutational burden, microsatellite instability, and lower survival rate across multiple tumors. Targeting CDK1 may provide a novel and effective strategy for cancer immunotherapy. Abstract Cyclin-dependent kinase 1 (CDK1) is essential for cell division by regulating the G2/M phase and mitosis. CDK1 overexpression can also promote the development and progression of a variety of cancers. However, the significance of CDK1 in the formation, progression, and prognosis of human pan-cancer remains unclear. In the present study, we used The Cancer Genome Atlas database, Clinical Proteomic Tumor Analysis Consortium, Human Protein Atlas, Genotype-Tissue Expression, and other well-established databases to comprehensively examine CDK1 genetic alterations and gene/protein expression in various cancers and their relationships with the prognosis, immune reactivities, and clinical outcomes for 33 tumor types. Gene set enrichment analysis was also conducted to examine the potential mechanisms of CDK1 in tumorigenesis. The data showed that CDK1 mutation was frequently present in multiple tumors. CDK1 expression was significantly increased in various types of tumors as compared with normal tissues and was associated with poor overall and disease-free survival. In addition, CDK1 expression was significantly correlated with oncogenic genes, proteins, cellular components, myeloid-derived suppressor cell infiltration, ESTMATEScore, and signaling pathways associated with tumor development and progression and tumor microenvironments. These data indicate that CDK1 could serve as a promising biomarker for predicting tumor prognosis and a potential target for cancer treatment.

Dataset Information

The M-phase specific hyperphosphorylation of Staufen2 involved the cyclin-dependent kinase CDK1.

Background

Results

Conclusions

Publications

The M-phase specific hyperphosphorylation of Staufen2 involved the cyclin-dependent kinase CDK1.

Similar Datasets

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