RSF1 functions as an oncogene in osteosarcoma and is regulated by XIST/miR-193a-3p axis

Wu, Dapeng; Nie, Xing‐Guo; Ma, Chao; Li, Xianghua; Li, Xue; An, Yongbo; Zhao, Bin; Wu, Xuejian

doi:10.1016/j.biopha.2017.08.068

Cited by 19 publications

(18 citation statements)

References 24 publications

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“…XIST acts as a molecular sponge for miR‐193a‐3p. XIST/miR‐193a‐3p/RSF1 axis might promote the progression and serve as a therapeutic target for OS patients (Wu et al, ). However, the role of miR‐193a‐3p has not been studied extensively.…”

Section: Discussionmentioning

confidence: 99%

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

Yang

et al. 2020

Cell Biology International

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Long non‐coding RNAs (lncRNAs) were reported to be involved in the progression of osteoarthritis (OA). The aim of this work was to explore the functional role of lncRNA nuclear‐enriched abundant transcript 1 (NEAT1) in OA. Reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of microRNA (miR‐193a)‐3p, NEAT1, and sex‐determining region Y‐box protein 5 (SOX5), as well as the levels of pro‐inflammatory cytokines interleukin‐6 (IL‐6), IL‐1β, tumor necrosis factor‐α (TNF‐α), and IL‐8 in OA cartilage tissue and chondrocytes. In addition, flow cytometry was used to measure the apoptosis of chondrocytes. The protein levels of extracellular matrix ACAN, collagen type II α1 chain (Col2a1), matrix metalloproteinase‐3 (MMP‐3), MMP‐13, a disintegrin, and metalloproteinase with thrombospondin motifs (ADAMTS)‐5 and SOX5 were determined using western blot analysis. Dual‐luciferase reporter assay was performed to determine the target relationship among NEAT1, miR‐193a‐3p, and SOX5. We found that miR‐193a‐3p expression was downregulated, while NEAT1 and SOX5 were upregulated in OA cartilage tissue and chondrocytes. Both upregulation of miR‐193a‐3p and knockdown of NEAT1 suppressed inflammation, apoptosis, and reduced the protein levels of MMP‐3, MMP‐13, and ADAMTS‐5, while elevating ACAN and Col2a1 expression in chondrocytes. NEAT1 targeted miR‐193a‐3p, and SOX5 was targeted by miR‐193a‐3p. Silencing of miR‐193a‐3p reversed the NEAT1 knockdown‐mediated effect on the inflammation, apoptosis, and production of the extracellular matrix. The introduction of SOX5 abolished the impact of the upregulation of miR‐193a‐3p on inflammation, apoptosis, and production of extracellular matrix in chondrocytes. In conclusion, NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human OA.

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Section: Discussionmentioning

confidence: 99%

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

Yang

et al. 2020

Cell Biology International

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“…The EC effects on the Erk and Akt pathways may also be linked to those on mir-193a and let-7g expression. Indeed, miR-193a was previously reported to be involved in the control of Akt [ 18 , 19 ] and Erk [ 20 ] signals in non-small-cell lung cancer and in colon cancer cells, respectively. Also, the let-7g regulated Akt pathway in gastric tumour [ 39 ] and several lines of evidence indicate these two miRNAs have a potential oncosuppressive role in melanoma since they are down-regulated in tissues and plasma of melanoma patients [ 40 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…These pathways are controlled of different intracellular molecules, among which are microRNAs (miRNAs), small non-coding RNAs that negatively regulate gene and other non-coding transcripts expression. Among the miRNAs affecting these pathways, are miR-193a-3p and let-7g-5p [ 18 , 19 , 20 ], which also promote apoptosis in cancer cells [ 21 , 22 ]. Therefore, in the present study, the effects of EC on Erk and Akt activation as well as on miR-193a and let-7g expression in melanoma cells were also investigated.…”

Section: Introductionmentioning

confidence: 99%

Anticancer Activity of Euplotin C, Isolated from the Marine Ciliate Euplotes crassus, Against Human Melanoma Cells

et al. 2018

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Cutaneous melanoma is the most serious type of skin cancer, so new cytotoxic weapons against novel targets in melanoma are of great interest. Euplotin C (EC), a cytotoxic secondary metabolite of the marine ciliate Euplotes crassus, was evaluated in the present study on human cutaneous melanoma cells to explore its anti-melanoma activity and to gain more insight into its mechanism of action. EC exerted a marked cytotoxic effect against three different human melanoma cell lines (A375, 501Mel and MeWo) with a potency about 30-fold higher than that observed in non-cancer cells (HDFa cells). A pro-apoptotic activity and a decrease in melanoma cell migration by EC were also observed. At the molecular level, the inhibition of the Erk and Akt pathways, which control many aspects of melanoma aggressiveness, was shown. EC cytotoxicity was antagonized by dantrolene, a ryanodine receptor (RyR) antagonist, in a concentration-dependent manner. A role of RyR as a direct target of EC was also suggested by molecular modelling studies. In conclusion, our data provide the first evidence of the anti-melanoma activity of EC, suggesting it may be a promising new scaffold for the development of selective activators of RyR to be used for the treatment of melanoma and other cancer types.

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“…The mechanisms underlying the pathogenesis of OS remains unclear. Studies have reported that a variety of oncogenes and tumor suppressor genes have significant contributions in the development of OS, but the specific molecular mechanisms remain unclear (6)(7)(8)(9). Therefore, a better understanding of the mechanisms underpinning the development of OS may provide an important theoretical basis for the clinical treatment of OS.…”

Section: Introductionmentioning

confidence: 99%

miR‑4295 promotes cell proliferation, migration and invasion of osteosarcoma through targeting interferon regulatory factor 1

et al. 2020

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Osteosarcoma (OS) is the most common form of primary malignant bone tumor. Despite encouraging progress in the treatment of OS, the survival rate for patients with OS has remained unchanged over the past 40 years. It has been established that miRNA plays a crucial regulatory role in the progression and development of OS. To explore the potential association of miRNAs with OS, bioinformatics techniques were used to screen for differentially expressed miRNA genes in OS in the Gene Expression Omnibus database. In the GSE70367 database, it was revealed that miR-4295 expression was abnormally elevated in the expression of OS cells. To characterize the potential function of miR-4295 in OS, the expression levels of miR-4295 in 30 samples of OS and adjacent normal tissues was examined. The results revealed that the expression of miR-4295 was significantly increased in OS tissues compared with the paired normal tissues. Moreover, the expression levels of miR-4295 in OS cell lines (MG-63 and Saos-2) were significantly higher compared with those in the normal human mesenchymal stem cells. In addition, miR-4295 was associated with OS cell proliferation, migration and invasion. Furthermore, it was demonstrated that the expression of interferon regulatory factor (IRF)1, a tumor suppressor, was regulated by miR-4295 directly in OS cells. Taken together, the present results revealed that miR-4295 may act as a tumor activator by target ing IRF1 during the progression of OS. Investigating miR-4295 may provide novel insight into the mechanisms of OS metastasis, and inhibition and targeting miR-4295 may be a novel therapeutic strategy for the treatment of OS.

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RSF1 functions as an oncogene in osteosarcoma and is regulated by XIST/miR-193a-3p axis

Cited by 19 publications

References 24 publications

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

NEAT1/miR‐193a‐3p/SOX5 axis regulates cartilage matrix degradation in human osteoarthritis

Anticancer Activity of Euplotin C, Isolated from the Marine Ciliate Euplotes crassus, Against Human Melanoma Cells

miR‑4295 promotes cell proliferation, migration and invasion of osteosarcoma through targeting interferon regulatory factor 1

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