MiR-17-5p modulates osteoblastic differentiation and cell proliferation by targeting SMAD7 in non-traumatic osteonecrosis

Jia, Jie; Feng, Xiaobo; Xu, Weihua; Yang, Shuai; Zhang, Qing; Liu, Xianzhe; Feng, Yong; Dai, Zhipeng

doi:10.1038/emm.2014.43

Cited by 97 publications

(73 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Of note, SMAD7 is also a potent regulator for cell proliferation [10,34]. Therefore, it may be interesting to analyze the coordinating role of CYLD and SMAD7 in the regulation of OSCC cell growth in the future study.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Oral Squamous Cell Carcinoma Proliferation Through Crosstalk Between SMAD7 and CYLD

2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: SMAD7 is a key inhibitor of transforming growth factor β (TGFβ) receptor signaling, which regulates the alteration of cancer cell invasiveness through epithelial-mesenchymal cell conversion. Dysfunction of protein ubiquitination plays a critical role in carcinogenesis, whereas the involvement a deubiquitinating enzyme, cylindromatosis gene (CYLD), in the tumor invasion of oral squamous cell carcinoma (OSCC) is unknown. Methods: Here, we studied the role of CYLD in regulation of OSCC cell invasion, using clinic specimens and cell lines. We modified SMAD7 levels in OSCC cells, and examined its effects on CYLD mRNA and protein levels by RT-qPCR and by Western blot, respectively. We also modified CYLD levels in OSCC cells, and examined its effects on SMAD7 mRNA and protein levels by RT-qPCR and by Western blot, respectively. Then, we examined the cell invasiveness in CYLD and/or SMAD7-modified OSCC cells in a transwell cell invasion assay. Results: We found that the levels of CYLD and SMAD7 were significantly decreased in OSCC specimens, compared to the paired normal tissue. Metastatic OSCC appeared to contained lower levels of CYLD and SMAD7. Moreover, CYLD and SMAD7 levels strongly correlated in OSCC specimens. Low CYLD levels were associated with poor patients' survival. Moreover, SMAD did not regulate CYLD, but CYLD regulated the levels of SMAD7 in OSCC cells. Furthermore, CYLD overexpression inhibited SMAD7-mediated cell invasion, while CYLD depletion increased SMAD7-mediated cell invasion in OSCC cells. Conclusion: Suppression of CYLD in OSCC cells may promote SMAD7-mediated cancer invasion. Thus, CYLD appears to be an intriguing therapeutic target to prevent OSCC metastases.

show abstract

Section: Discussionmentioning

confidence: 99%

Regulation of Oral Squamous Cell Carcinoma Proliferation Through Crosstalk Between SMAD7 and CYLD

2016

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…8,[31][32][33][34] In this study, we performed miRNA microarray to identify the differentially abundant miRNAs in the serums of SLE patients with steroidinduced ONFH as compared with SLE control and healthy control groups. Our data indicated that miR-4440 was commonly increased,…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNA signature of steroid‐induced osteonecrosis of the femoral head

Zheng

Jiang

et al. 2017

Cell Proliferation

View full text Add to dashboard Cite

ObjectivesSteroid‐induced osteonecrosis of the femoral head (ONFH) is a common orthopaedic disease of which early detection remains clinically challenging. Accumulating evidences indicated that circulating microRNAs (miRNAs) plays vital roles in the development of several bone diseases. However, the association between circulating miRNAs and steroid‐induced ONFH remains elusive.Materials and methodsmiRNA microarray was performed to identify the differentially abundant miRNAs in the serums of systemic lupus erythematosus (SLE) patients with steroid‐induced ONFH as compared with SLE control and healthy control group. We predicted the potential functions of these differentially abundant miRNAs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses and reconstructed the regulatory networks of miRNA‐mRNA interactions.ResultsOur data indicated that there were 11 differentially abundant miRNAs (2 upregulated and 9 downregulated) between SLE‐ONFH group and healthy control group and 42 differentially abundant miRNAs (14 upregulated and 28 downregulated) between SLE‐ONFH group and SLE control group. We also predicted the potential functions of these differentially abundant miRNAs using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses and reconstructed the regulatory networks of miRNA‐mRNA interactions.ConclusionsThese findings corroborated the idea that circulating miRNAs play significant roles in the development of ONFH and may serve as diagnostic markers and therapeutic targets.

show abstract

“…Furthermore, miR-17-5p overexpression promotes osteogenic differentiation of MSCs (mesenchymal stem cells) [35]. However, during aging and in pro-inflammatory diseases, miR-17-5p expression was observed low in MSCs, concomitant with compromised osteogenic differentiation [36].…”

Section: Aging the Mir-17-92 Cluster And Mir-17-5pmentioning

confidence: 99%

MicroRNA-17-5p: At the Crossroads of Cancer and Aging - A Mini-Review

Dellago

Bobbili²,

Grillari³

2016

Gerontology

View full text Add to dashboard Cite

The miR-17-92 cluster, led by its most prominent member, miR-17-5p, has been identified as the first miRNA with oncogenic potential. Thus, the whole cluster containing miR-17-5p has been termed oncomiR-1. It is strongly expressed in embryonic stem cells and has essential roles in vital processes like cell cycle regulation, proliferation and apoptosis. The importance of miR-17-5p for fundamental biological processes is underscored by the fact that a miR17-deficient mouse is neonatally lethal. Recently, miR-17-5p was identified in the context of aging, since it is comprised in a common signature of miRNAs that is downregulated in several models of aging research. Recently, miR-17-5p turned out to be the first ‘longevimiR' in an animal model, extending the lifespan of a transgenic miR-17-5p-overexpressing mouse. Here, we summarize the current status of research on miR-17-5p with emphasis on its role in cellular senescence, aging and cancer, which points to a pleiotropic function of miR-17-5p regulating multiple targets involved in autophagy, cell cycle regulation and apoptosis in a tissue-dependent fashion. In addition, its elevated presence in serum or plasma of a wide range of tumor patients suggests using it as an ‘alarmiR', a general indicator of a potential tumor pathology. However, amounts of circulating miR-17-5p of healthy individuals as reference values are still missing, before any miRNA can be classified as such an ‘alarmiR'. In conclusion, miR-17-5p is at the crossroads of aging, longevity and cancer and might represent a promising biomarker or even therapeutic tool and target in this context.

show abstract

MiR-17-5p modulates osteoblastic differentiation and cell proliferation by targeting SMAD7 in non-traumatic osteonecrosis

Cited by 97 publications

References 24 publications

Regulation of Oral Squamous Cell Carcinoma Proliferation Through Crosstalk Between SMAD7 and CYLD

Regulation of Oral Squamous Cell Carcinoma Proliferation Through Crosstalk Between SMAD7 and CYLD

Circulating microRNA signature of steroid‐induced osteonecrosis of the femoral head

MicroRNA-17-5p: At the Crossroads of Cancer and Aging - A Mini-Review

Contact Info

Product

Resources

About