The Role of miRNA in the Diagnosis, Prognosis, and Treatment of Osteosarcoma

Wang, Jicheng; Liu, Shizhang; Shi, Jiyuan; Li, Jinyuan; Wang, Songbo; Liu, Huitong; Zhao, Song; Duan, Keke; Pan, Xuezhen; Zhi, Yi

doi:10.1089/cbr.2019.2939

Cited by 77 publications

(63 citation statements)

References 69 publications

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“…MicroRNAs (miRNAs) are small single-stranded noncoding RNAs with apoptosis-promoting or antiapoptotic roles, consisting of 20-26 nucleotides [11]. MiRNAs inhibited gene expression through binding to the 3′ untranslated regions (3'UTR) of their target mRNAs [12]. There is growing evidence that miRNAs play key roles in IVDD and miR-199a was associated with clinical grades of degeneration [13].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

et al. 2020

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Background: Intervertebral disc degeneration (IVDD) is a well-known cause of lower back pain, which is induced by multiple factors including increased apoptosis and decreased survival of nucleus pulposus cells. In this study, we evaluate the effect and potential mechanism of miR-660 on the nucleus pulposus cells apoptosis induced by TNF-α. Methods: First, we collected tissue of nucleus pulposus from IVDD and healthy controls. General characteristic of the IVDD and healthy control was also collected. And, we also collected nucleus pulposus cells that stimulated by TNF-α or control. miRNA microarray was performed to identify the differentially expressed miRNAs. Apoptosis rate and miR-660 relative expression was measured after stimulated with different concentration of TNF-α to identify the optimal concentration of TNF-α. Second, we successfully constructed antigomiR-660 to block the miR-660 expression in nucleus pulposus cells and then stimulated with TNF-α (100 ng/ml, 12 h). The apoptosis rates and relative protein expression were then measured again. The target association between miR-660 and SAA1 was confirmed by dual-luciferase reporter. Results: There was no significant difference between the age (IVDD: 39 ± 10 years, healthy controls: 36 ± 7 years), BMI and sex between IVDD and healthy controls. Microarray analysis found that miR-660 was significantly upregulated in IVDD and TNF-α treated groups, which was further identified by PCR. We found that the rate of apoptosis and miR-660 expression increased with TNF-α concentration increased. Finally, TNF-a with 100 ng/ml was used for further experiment. Compared with TNF-α group, TNF-α + antigomiR-660 could significantly downregulated the apoptosis rate and relative protein (c-Caspase3 and c-Caspase7). Dual-luciferase reporter revealed that miR-660 could directly binding to the SAA1 at 80-87 sites. Compared with TNF-α alone group, TNF-α + antigomiR-660 significantly up-regulated the SAA1 expression (P < 0.05). Conclusion: These results indicated that knockdown of miR-660 protected the nucleus pulposus from apoptosis that induced TNF-α via up-regulation of SAA1. Further studies should focus on the role of miR-660 in protecting IVDD in vivo.

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Section: Introductionmentioning

confidence: 99%

Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

et al. 2020

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“…MicroRNAs (miRNAs) have attracted major interest due to their ability to affect a wide range of fundamental biological processes such as proliferation, invasion, differentiation and apoptosis (5). Studies into OS-specific miRNAs have identified their potential in the prevention and management of OS (6,7). Based on the latest version of miRBase, ~3,700 miRNAs loci were annotated in human tissues (8).…”

Section: Introductionmentioning

confidence: 99%

miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

He¹,

Chen²,

Liu³

et al. 2020

Exp Ther Med

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MicroRNA (miR)-106b-5p has been reported to act as both an oncogene and tumor suppressor in several tumors. The aim of the present study was to investigate the biological function of miR-106b-5p in osteosarcoma (OS). miR-106b-5p expression was observed to be significantly increased in OS tissues and cell lines. MTT assay and flow cytometry analysis determined that miR-106b-5p inhibitor transfection suppressed OS cell proliferation and induced cell cycle G0/G1 phase arrest. Furthermore, bioinformatics analysis and a luciferase reporter assay demonstrated that cyclin-dependent kinase inhibitor 1A (CDKN1A) was a potential target of miR-106b-5p. p21 protein expression was found to be significantly increased by miR-106b-5p downregulation in OS cells. Further analysis demonstrated that CDKN1A was downregulated in OS tissues and was negatively correlated with miR-106b-5p expression. Furthermore, upregulation of CDKN1A expression mimicked, whilst CDKN1A knockdown reversed the suppressive effects of miR-106b-5p inhibitor on OS cell proliferation and cell cycle progression. In summary, the present data suggested that miR-106b-5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in OS.

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“…Notably, miRNA dysregulation contributes to the development and progression of various tumours, including osteosarcoma 29,30 . These miRNAs can be used as potential biomarkers for diagnosis and prognosis, and therapeutic targets for treatment of osteosarcoma 31 …”

Section: Introductionmentioning

confidence: 99%

PTPN14, a target gene of miR‐4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling

Liang

Duan

et al. 2020

Clin Exp Pharma Physio

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Non-receptor tyrosine phosphatase 14 (PTPN14) has emerged as a novel tumoursuppressor in a wide range of human cancer types. However, the role of PTPN14 in osteosarcoma remains undetermined. In the present study, we aimed to explore the expression pattern, biological function, and regulation of PTPN14 in osteosarcoma.Low PTPN14 expression levels were detected in osteosarcoma cells, and PTPN14 overexpression markedly decreased the proliferation, colony formation, and invasive potential of osteosarcoma cells. Bioinformatics analysis predicted PTPN14 as a potential target gene of microRNA-4295 (miR-4295), and this prediction was validated by a dual-luciferase reporter assay. PTPN14 expression was negatively modulated by miR-4295 in osteosarcoma cells. Moreover, PTPN14 expression was inversely correlated with miR-4295 expression in osteosarcoma tissues. Notably, miR-4295 inhibition significantly restricted the proliferation and invasion of osteosarcoma cells. PTPN14 overexpression or miR-4295 inhibition increased the phosphorylation ofYes-associated protein 1 (YAP1) and impeded YAP1 nuclear translocation, leading to inhibition of YAP1-mediated transcriptional activity. However, the miR-4925-inhibition-mediated antitumour effect was partially reversed by PTPN14 knockdown.Overall, these results demonstrate that PTPN14 is a miR-4295 target gene and it exerts a tumour-suppressive function in osteosarcoma cells via inactivation of YAP1.Our study uncovers a miR-4295-PTPN14-YAP1 signalling pathway that may play a crucial role in the progression of osteosarcoma. K E Y W O R D S miR-4295, osteosarcoma, PTPN14, YAP1 S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Liang G, Duan C, He J, Ma W, Dai X. PTPN14, a target gene of miR-4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling.

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The Role of miRNA in the Diagnosis, Prognosis, and Treatment of Osteosarcoma

Cited by 77 publications

References 69 publications

Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

Knockdown of miR-660 protects nucleus pulposus cells from TNF-a-induced apoptosis by targeting serum amyloid A1

miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

PTPN14, a target gene of miR‐4295, restricts the growth and invasion of osteosarcoma cells through inactivation of YAP1 signalling

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