Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

Ni, Zhaohui; Xf, Shang; Wang, Yafang; Sun, Yi-Chih; Dj, Fu

doi:10.4238/gmr.15027807

Cited by 19 publications

(10 citation statements)

References 31 publications

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“…Certain microRNAs can promote the tumorigenesis of osteosarcoma. Ni et al ( 11 ) found that miR-301a is frequently upregulated in osteosarcoma and that aberrant expression of miR-301a promotes the proliferation of osteosarcoma cell lines. miR-17-5p has also shown diagnostic and prognostic significance in osteosarcoma, as the overexpression of miR-17-5p substantially promotes malignant phenotypes ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-643 regulates the expression of ZEB1 and inhibits tumorigenesis in osteosarcoma

Wang

Xing

Ren

et al. 2017

Molecular Medicine Reports

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Osteosarcoma is among the most malignant types of tumor worldwide and has become a leading contributor to tumor incidence, particularly in adolescents. Resistance to conventional treatment and the complexity of osteosarcoma tumorigenesis has resulted in high mortality rates. MicroRNAs are a class of noncoding RNAs, which regulate numerous biological processes. However, the involvement of miR-643 in osteosarcoma remains to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction, luciferase reporter assay, invasion assay, viability assay, western blot analysis and in vivo implantation were performed to analyze the action of miR-643 in osteosarcoma. The results demonstrated that miR-643 inhibited the progression of osteosarcoma and acted as a potential tumor suppressor. The expression of miR-643 was downregulated in osteosarcoma tissues and cell lines. In addition, miR-643 transfection significantly impaired the proliferation and invasion of osteosarcoma cells. The present study also identified Zinc finger E-box-binding homeobox 1 (ZEB1) as a direct target of miR-643, and the ectopic expression of ZEB1 counteracted the effect of miR-643 transfection. A significant inverse correlation was also found between the expression of miR-643 and ZEB1. A low expression of miR-643 or a high expression of ZEB1 was associated with poor patient survival rates. The results of the present study suggested that the decreased expression of miR-643 may be involved in the mechanism underlying the development of osteosarcoma. The intricate interactions between miR-643 and ZEB1 may serve as a potential therapeutic target in osteosarcoma oncogenesis.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-643 regulates the expression of ZEB1 and inhibits tumorigenesis in osteosarcoma

Wang

Xing

Ren

et al. 2017

Molecular Medicine Reports

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“…Although AML is a relatively rare disease, accounting for ~1.2% of cases of cancer-associated mortality, its incidence is expected to increase as the population ages (20). Several miRNAs are located inside or close to chromosomal fragile sites, which are frequently lost or amplified in cancer, and the correlation between miRNAs and cancer has become a focus for the diagnosis and therapy of cancer (21,22). In the present study, it was demonstrated that the expression of miR-21 was significantly increased in peripheral blood monocytes of patients with AML, compared with healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR‑21 is involved in acute monocytic leukemia‑associated angiogenesis by targeting IL‑12

Chen

Yang

et al. 2018

Mol Med Report

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Angiogenesis is important in pathophysiological processes, including the pathogenesis of acute monocytic leukemia (AML). MicroRNA‑21 (miR‑21) is overexpressed and exhibits oncogenic activity in cancer. However, the biological mechanism underlying the effect of miR‑21 in AML remains to be fully elucidated. In the present study, the expression levels of miR‑21 and vascular endothelial growth factor (VEGF) were determined in 26 patients with AML and 28 healthy individuals. The secretion of VEGF was also measured following the transfection of THP‑1 cells with miR‑21 mimic or inhibitor. The supernatants of the THP‑1 cells, which were transfected with miR‑21 mimic, inhibitor or small interfering RNA (si)VEGF, respectively, were used to incubate human umbilical vein endothelial cells (HUVECs), following which tube formation of the HUVECs was measured. miR‑21 targets were predicted using a biological target prediction website and confirmed using a luciferase assay. The effects of interleukin (IL)‑12 were investigated by examining the tube formation of HUVECs and the secretion of VEGF following recombinant human (rh) IL‑12 pretreatment. The results revealed that miR‑21 and VEGF expression was significantly increased in the peripheral blood monocytes of the patients, compared with the healthy controls. There was negative correlation between the expression of IL‑12 and miR‑21 in the serum of patients with AML. Furthermore, supernatant VEGF levels from the miR‑21 mimic‑transfected THP‑1 cells were increased, whereas a decreasing trend was observed in the miR‑21 inhibitor group. The angiogenic ability of the HUVECs pretreated with supernatant from the THP‑1 cells transfected with miR‑21 mimic was higher, and was lower in THP‑1 cells co‑transfected with miR‑21 mimic and siVEGF, compared with the miR‑21 mimic only group. A luciferase assay demonstrated that IL‑12 was the direct target of miR‑21, and the level of IL‑12 in the supernatant of THP‑1 cells transfected with miR‑21 mimic was increased. IL‑12 pretreatment increased VEGF expression and angiogenic ability in HUVECs. The inactivation of miR‑21 or activation of its target gene may be a potential therapeutic strategy in human AML.

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“…Although Fenger et al investigated on miR-9 in OS, Ni et al showed not only that miR-301a is overexpressed in OS cell lines but also that this miRNA enhances cell migration and inhibits apoptosis [ 192 ]. Therefore, they confirmed the carcinogenic function of miR-301a in OS, which was only observed in others cancers [ 193 , 194 ].…”

Section: Mirnas and Primary Bone Tumoursmentioning

confidence: 99%

What Is New in the miRNA World Regarding Osteosarcoma and Chondrosarcoma?

2017

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Despite the availability of multimodal and aggressive therapies, currently patients with skeletal sarcomas, including osteosarcoma and chondrosarcoma, often have a poor prognosis. In recent decades, advances in sequencing technology have revealed the presence of RNAs without coding potential known as non-coding RNAs (ncRNAs), which provides evidence that protein-coding genes account for only a small percentage of the entire genome. This has suggested the influence of ncRNAs during development, apoptosis and cell proliferation. The discovery of microRNAs (miRNAs) in 1993 underscored the importance of these molecules in pathological diseases such as cancer. Increasing interest in this field has allowed researchers to study the role of miRNAs in cancer progression. Regarding skeletal sarcomas, the research surrounding which miRNAs are involved in the tumourigenesis of osteosarcoma and chondrosarcoma has rapidly gained traction, including the identification of which miRNAs act as tumour suppressors and which act as oncogenes. In this review, we will summarize what is new regarding the roles of miRNAs in chondrosarcoma as well as the latest discoveries of identified miRNAs in osteosarcoma.

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Upregulated microRNA-301a in osteosarcoma promotes tumor progression by targeting CDC14A

Cited by 19 publications

References 31 publications

MicroRNA-643 regulates the expression of ZEB1 and inhibits tumorigenesis in osteosarcoma

MicroRNA-643 regulates the expression of ZEB1 and inhibits tumorigenesis in osteosarcoma

Overexpression of miR‑21 is involved in acute monocytic leukemia‑associated angiogenesis by targeting IL‑12

What Is New in the miRNA World Regarding Osteosarcoma and Chondrosarcoma?

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