Demethylation of microRNA-142 induced by demethylation agents plays a suppressive role in osteosarcoma cells

Ding, Muliang; Hu, Jianzhong; Ni, Jiangdong; Zheng, Ziming; Song, Deye; Wang, Junjie

doi:10.3892/ol.2015.3036

Cited by 7 publications

(10 citation statements)

References 34 publications

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“…The associations between miR-142-mediated proliferation and apoptosis signaling have been previously reported in OS. As previous study reported, miR-142 can mediates cancer cell proliferation and apoptosis in OS ( 11 , 13 , 31 , 32 ). Ding et al ( 31 ) reported that the expression level of miR-142 was significantly lower in OS tissues and cells due to hypermethylation, suggesting that miR-142 served an important role in the inhibition of the proliferation, and invasiveness of OS cell lines induced by demethylation agents.…”

Section: Discussionsupporting

confidence: 52%

“…As previous study reported, miR-142 can mediates cancer cell proliferation and apoptosis in OS ( 11 , 13 , 31 , 32 ). Ding et al ( 31 ) reported that the expression level of miR-142 was significantly lower in OS tissues and cells due to hypermethylation, suggesting that miR-142 served an important role in the inhibition of the proliferation, and invasiveness of OS cell lines induced by demethylation agents. Xu et al ( 11 ) has identified that overexpression of miR-142-3p in OS cells suppressed cell proliferation, migration and invasion by directly targeting HMGA1.…”

Section: Discussionsupporting

confidence: 52%

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miR‑142 suppresses proliferation and induces apoptosis of osteosarcoma cells by upregulating Rb

Gao

Zhang

et al. 2018

Oncol Lett

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It has been reported that microRNA-142 (miR-142) is a tumor suppressor gene. The present study primarily investigated whether the overexpression of miR-142 was able to inhibit the proliferation, apoptosis and expression of apoptosis-associated proteins in osteosarcoma (OS) cells. Different concentrations of miR-142 were transfected into the OS MG-63 cell line using Lipofectamine 2000. The cell lines were divided into three groups: Normal group (non-transfected group), miR-142 transfected group, and negative group, which were transfected with random miR-142 fragment. The proliferation of cells was detected by MTT assay. The expression of miR-142 was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). DAPI staining was performed to investigate the influence of miR-142 on the morphology of MG-63c ells. The apoptotic cell percentages were determined by flow cytometry with Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Expression of tumor suppressors, phosphatase and tensin homolog (PTEN) and Retinoblastoma-associated protein (Rb), and apoptosis-associated proteins were evaluated by western blotting. RT-qPCR indicated a higher expression of miR-142 in the transfected group (miR-142 was transfected into the MG-63 cell line) compared with that in the normal (non-transfected group) and negative control groups. The proliferation of miR-142 transfected cells was significantly lower compared with that in the normal and negative groups. Furthermore, an increased apoptosis rate accompanied by a statistically significant upregulation of PTEN, Rb phosphorylation, cleaved caspase-3 and cytochrome c protein levels were detected in the transfected group, indicating an internal apoptosis pathway was involved in this process. Furthermore, no significant changes were identified between the normal and negative groups (P>0.05). The present study demonstrated that miR-142 overexpression by liposomal transfection resulted in an inhibitory effect on MG-63 cell proliferation. The underlying mechanisms may relate to the upregulation of tumor suppressor and activation of caspase signaling pathway, which may provide a novel horizon in short nucleotide drugs on the management of OS.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionsupporting

confidence: 52%

miR‑142 suppresses proliferation and induces apoptosis of osteosarcoma cells by upregulating Rb

Gao

Zhang

et al. 2018

Oncol Lett

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“…In the present study, we first confirmed that miR-138 is downregulated in osteosarcoma tissues and cell lines. Different miRNA expression profiles in osteosarcoma have been identified previously [ 17 – 19 ]. MiR-138 plays important roles different cancers.…”

Section: Discussionmentioning

confidence: 99%

MiR-138 Acts as a Tumor Suppressor by Targeting EZH2 and Enhances Cisplatin-Induced Apoptosis in Osteosarcoma Cells

et al. 2016

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Chemotherapeutic insensitivity remains a major obstacle to treating osteosarcoma effectively. Recently, increasing evidence has suggested that microRNAs (miRNAs) are involved in drug resistance. However, the effect of miR-138 on cisplatin chemoresistance in osteosarcoma has not been reported. We used real-time PCR to detect the expression of mature miR-138 in osteosarcoma tissues and cell lines. Cell proliferation, invasion, and migration assays were used to observe changes to the osteosarcoma malignant phenotype. MiR-138 was downregulated in osteosarcoma tissues and cell lines, and miR-138 overexpression negatively regulated osteosarcoma cell proliferation, migration, and invasion. We also verified that EZH2 is a direct target of miR-138. Furthermore, enhancing EZH2 expression reduced the inhibitory effects of miR-138 on osteosarcoma. Proliferation, apoptosis assays and caspase-3 activity assay confirmed that elevated miR-138 expression enhanced osteosarcoma cell chemosensitivity to cisplatin by targeting EZH2. In conclusion, the present study demonstrates that miR-138 acts as a tumor suppressor by enhancing osteosarcoma cell chemosensitivity and supports its potential application for treating osteosarcoma in the future.

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“…Accumulating evidence suggested that miRs may act as oncogenes or tumor suppressor genes by regulating their targets, most of which were the key regulators in the process of cell proliferation, apoptosis, metastasis and angiogenesis [ 10 ]. Previous studies have identified that miR-142 plays a critical role in the development of a variety of cancers such as osteosarcoma and renal cancer [ 11 , 12 ]. However, the expression and function of miR-142 in HCC still remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Over-expression of Thrombospondin 4 correlates with loss of miR-142 and contributes to migration and vascular invasion of advanced hepatocellular carcinoma

Zhao

Qin

et al. 2017

Oncotarget

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Hepatocellular carcinoma (HCC) is a common malignancy found worldwide and is associated with a high incidence of metastasis and vascular invasion. Elucidating the molecular mechanisms that underlie HCC tumorigenesis and progression is necessary for the development of novel therapeutics. By analyzing the Cancer Genome Atlas Network (TCGA) dataset, we identified Thrombospondin 4 (THBS4) is significantly overexpressed in HCC samples and is correlated with prognosis. Overexpression of THBS4 was also highly correlated with vascular invasion of advanced HCC. While THBS4 is often overexpressed in HCC it has also been shown to inhibit tumor growth by mediating cell-to-cell and cell-to-matrix interactions. Here, we identified that knockdown of THBS4 inhibits migration and invasion of HCC cells and inhibits HCC induced angiogenesis. MiRNAs are crucial regulators of multiple cellular processes, and aberrant expression of miRNAs has been observed to effect cancer development and progression. We further found that miR-142 is an upstream regulator of THBS4 in HCC cells. Moreover, miR-142 was significantly down-regulated in HCC tissue samples and correlated with overexpression of THBS4. Overexpression of miR-142 inhibited invasion and angiogenesis of HCC cells and re-expression of THBS4 overcame these effects of miR-142 expression. Stable over-expression of miR-142 significantly inhibited tumour growth in a xenograft tumour model through inhibiting THBS4 expression and tumor angiogenesis. In conclusion, our findings indicate that loss of miR-142 results in the over-expression of THBS4, which enhances HCC migration and vascular invasion. Thus, targeting THBS4 or miR-142 may provide a promising therapeutic strategy for treatment of advanced HCC.

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Demethylation of microRNA-142 induced by demethylation agents plays a suppressive role in osteosarcoma cells

Cited by 7 publications

References 34 publications

miR‑142 suppresses proliferation and induces apoptosis of osteosarcoma cells by upregulating Rb

miR‑142 suppresses proliferation and induces apoptosis of osteosarcoma cells by upregulating Rb

MiR-138 Acts as a Tumor Suppressor by Targeting EZH2 and Enhances Cisplatin-Induced Apoptosis in Osteosarcoma Cells

Over-expression of Thrombospondin 4 correlates with loss of miR-142 and contributes to migration and vascular invasion of advanced hepatocellular carcinoma

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