Progress in understanding the molecular functions of DDX3Y (DBY) in male germ cell development and maintenance

Kotov, A. A.; Olenkina, Oxana M.; Godneeva, Baira; Adashev, Vladimir E; Olenina, Ludmila V.

doi:10.5582/bst.2016.01216

Cited by 32 publications

(26 citation statements)

References 49 publications

(69 reference statements)

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“…The human genome code for two types of functional DDX3 genes, including DDX3X and its homolog DDX3Y (4). DDX3Y is located on the Y-chromosome, and plays particular roles of spermatogenesis and male fertility (5). While DDX3X is located on the X-chromosome and widely expresses in a broad range of organisms.…”

Section: Introductionmentioning

confidence: 99%

A double-edged function of DDX3, as an oncogene or tumor suppressor, in cancer progression (Review)

Zhang

Yang

et al. 2018

Oncol Rep

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DEAD-box RNA helicase 3 (DDX3) is a highly conserved family member of DEAD-box proteins in all eukaryotes from yeasts to human beings. Accumulating studies have confirmed DDX3 has the ability to regulate different steps of RNA metabolism, including RNA splicing, RNA export, transcription and translation initiation. Moreover, DDX3 is involved in many biological processes, such as stress response, cell apoptosis, cell cycle regulation and virus infection. In recent years, DDX3 is getting increasing attention due to its essential roles in cancer progression. However, DDX3 role in cancer development is rather complicated. This review mainly focuses on the dual roles of DDX3 and DDX3-mediated signaling pathways in multiple cancers. In addition, the interplaying causes for the controversial roles of DDX3 in cancer are discussed. So far several small molecular chemical compounds targeting DDX3 are also summarized from the anticancer activity to the clinical trials of DDX3 inhibitors.

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Section: Introductionmentioning

confidence: 99%

A double-edged function of DDX3, as an oncogene or tumor suppressor, in cancer progression (Review)

Zhang

Yang

et al. 2018

Oncol Rep

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“…Deficiency of bel leads to severe depletion of early germ cells via apoptosis in the testes of adult males, while somatic cyst cells and hub cells are still maintained [25]. This developmental disorder recapitulates the SCOS phenotype in humans with DBY gene deletions and also leads to severe male sterility [25,29]. Belle functions as an upstream regulator of expression of mitotic cyclins A and B both in the testes and ovaries [25,26].…”

Section: Introductionmentioning

confidence: 82%

The Drosophila RNA Helicase Belle (DDX3) Non-Autonomously Suppresses Germline Tumorigenesis Via Regulation of a Specific mRNA Set

Kotov

Godneeva

Olenkina

et al. 2020

Cells

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DDX3 subfamily DEAD-box RNA helicases are essential developmental regulators of RNA metabolism in eukaryotes. belle, the single DDX3 ortholog in Drosophila, is required for fly viability, fertility, and germline stem cell maintenance. Belle is involved both in translational activation and repression of target mRNAs in different tissues; however, direct targets of Belle in the testes are essentially unknown. Here we showed that belle RNAi knockdown in testis cyst cells caused a disruption of adhesion between germ and cyst cells and generation of tumor-like clusters of stem-like germ cells. Ectopic expression of β-integrin in cyst cells rescued early stages of spermatogenesis in belle knockdown testes, indicating that integrin adhesion complexes are required for the interaction between somatic and germ cells in a cyst. To address Belle functions in spermatogenesis in detail we performed cross-linking immunoprecipitation and sequencing (CLIP-seq) analysis and identified multiple mRNAs that interacted with Belle in the testes. The set of Belle targets includes transcripts of proteins that are essential for preventing the tumor-like clusters of germ cells and for sustaining spermatogenesis. By our hypothesis, failures in the translation of a number of mRNA targets additively contribute to developmental defects observed in the testes with belle knockdowns both in cyst cells and in the germline.

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“…A study by Jia et al26 showed that miR-212-5p suppressed the over-expression of COPD related genes, whereas CSE upregulated these genes. DDX3Y encodes an RNA helicase of the big DDX3 subfamily of the DEAD-box family of proteins 27. Furthermore, we concluded that DDX3Y was a target gene of miR-497 for the first time and was negatively modulated by miR-497.…”

mentioning

confidence: 80%

“…DDX3Y encodes an RNA helicase of the big DDX3 subfamily of the DEAD-box family of proteins. 27 As a part of the process of autosomal translocation, DDX3 genes present on mammalian sex chromosomes. 28 By reprogramming the chromosomes specifically, DDX3X and DDX3Y are localized to the non-recombinant portions of both sex chromosomes.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐497 functions as an inflammatory suppressor via targeting DDX3Y and modulating toll‐like receptor 4/NF‐κB in cigarette smoke extract‐stimulated human bronchial epithelial cells

Jia

Zhao

2019

The Journal of Gene Medicine

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Background:We aimed to investigate the biological effect of miR-497 in cigarette smoke extract (CSE)-damaged human bronchial epithelial (HBE) cells and the underlying molecular mechanism.Methods: MiR-497 mimic was transfected into HBE cells to up-regulate miR-497 expression. Cigarette smoke extract (CSE, 20 μg/mL) was utilized to treat HBE cells to form the injury model. Cell proliferation and apoptosis were detected by CCK8 and flow cytometry assays. DDX3Y mRNA expression was determined by a quantitative reverse transcriptase-polymerase chain reaction. The interaction between miR-497 and DDX3Y was verified by a luciferase reporter assay. Protein expression levels were tested by western blotting.Results: CSE treatment decreased miR-497 level in HBE cells. CSE exposure restrained cell proliferation, promoted cell apoptosis and enhanced the relative expression of TLR4 and p-NF-κB p65. DDX3Y was predicted as a target of miR-497. The mRNA and protein expression of DDX3Y was negatively modulated by miR-497 in CSE-injured HBE cells. Up-regulation of miR-497 by miR-497 mimic increased cell proliferation and reduced cell apoptosis in CSE-treated HBE cells, which were rescued by DDX3Y high expression in CSE-treated HBE cells. Consistently, Bcl-2 protein level was heightened, whereas Bax and actived caspase-3/9 protein levels were decreased by miR-497 mimic in CSE-stimulated HBE cells, which was reversed by DDX3Y over-expression in CSE-stimulated HBE cells. The relative expression of TLR4 and p-NF-κB p65 was decreased by miR-497 mimic, whereas they were rescued by DDX3Y over-expression in CSE-damaged HBE cells. Conclusions:The results of the present study demonstrate that up-regulation of miR-497 exhibits a protective effect on CSE-damaged HBE cells, which might be achieved by targeting DDX3Y and regulating the TLR4/NF-κB pathway. KEYWORDSchronic obstructive pulmonary disease, cigarette smoke extract, DEAD-box helicase 3 Y-linked, human bronchial epithelial cells, miR-497, Toll-like receptor 4/NF-ĸB pathway

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Progress in understanding the molecular functions of DDX3Y (DBY) in male germ cell development and maintenance

Cited by 32 publications

References 49 publications

A double-edged function of DDX3, as an oncogene or tumor suppressor, in cancer progression (Review)

A double-edged function of DDX3, as an oncogene or tumor suppressor, in cancer progression (Review)

The Drosophila RNA Helicase Belle (DDX3) Non-Autonomously Suppresses Germline Tumorigenesis Via Regulation of a Specific mRNA Set

MicroRNA‐497 functions as an inflammatory suppressor via targeting DDX3Y and modulating toll‐like receptor 4/NF‐κB in cigarette smoke extract‐stimulated human bronchial epithelial cells

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