lncRNA SNHG1 negatively regulates miRNA‑101‑3p to enhance the expression of ROCK1 and promote cell�proliferation, migration and invasion in osteosarcoma

Deng, Rui; Zhang, Jinyuan; Chen, Jianting

doi:10.3892/ijmm.2018.4039

Cited by 40 publications

(45 citation statements)

References 39 publications

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“…LncRNAs are transcribed with more than 200 nucleotides that play critical roles in different biological processes such as cell growth, transcription, and translation, epigenetic regulation of gene expression, splicing, nuclear cytoplasmic traffic, and cell cycle control (108). Recent studies show that lncRNAs can epigenetically regulate oncogenesis, which can prevent (109) favoring initiation and progression of OS (110,111). Thus, lncRNAs can contribute to the development and progression of OS by acting as tumor suppressors or as oncogenes inducing tumor formation (109,111).…”

Section: Role Of Non-coding Rnasmentioning

confidence: 99%

Biology and pathogenesis of human osteosarcoma (Review)

Azevedo¹,

Fernandes

et al. 2019

Oncol Lett

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Osteosarcoma (OS) is a bone tumor of mesenchymal origin, most frequently occurring during the rapid growth phase of long bones, and usually located in the epiphyseal growth plates of the femur or the tibia. Its most common feature is genome disorganization, aneuploidy with chromosomal alterations, deregulation of tumor suppressor genes and of the cell cycle, and an absence of DNA repair. This suggests the involvement of surveillance failures, DNA repair or apoptosis control during osteogenesis, allowing the survival of cells which have undergone alterations during differentiation. Epigenetic events, including DNA methylation, histone modifications, nucleosome remodeling and expression of non-coding RNAs have been identified as possible risk factors for the tumor. It has been reported that p53 target genes or those genes that have their activity modulated by p53, in addition to other tumor suppressor genes, are silenced in OS-derived cell lines by hypermethylation of their promoters. In osteogenesis, osteoblasts are formed from pluripotent mesenchymal cells, with potential for self-renewal, proliferation and differentiation into various cell types. This involves complex signaling pathways and multiple factors. Any disturbance in this process can cause deregulation of the differentiation and proliferation of these cells, leading to the malignant phenotype. Therefore, the origin of OS seems to be multifactorial, involving the deregulation of differentiation of mesenchymal cells and tumor suppressor genes, activation of oncogenes, epigenetic events and the production of cytokines. Contents 1. Introduction 2. Biology of human OS 3. Role of differentiation of mesenchymal stem cells 4. Role of DNA changes 5. Role of deregulating the expression of tumor suppressor genes 6. Regulation of oncogene expression 7. Role of epigenetic mechanisms 8. Role of non-coding RNAs 9. Role of cytokines 10. Conclusion

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Section: Role Of Non-coding Rnasmentioning

confidence: 99%

Biology and pathogenesis of human osteosarcoma (Review)

Azevedo¹,

Fernandes

et al. 2019

Oncol Lett

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“…Originally, it was shown that a few lncRNAs are abnormally expressed in osteosarcoma (Li et al, 2013;Li et al, 2016). Subsequently, a large number of lncRNAs have been demonstrated to play an important role in the activities of osteosarcoma (Li et al, 2018;Huang et al, 2018;Deng et al, 2019). Furthermore, some lncRNAs have been demonstrated to be associated with the chemoresistance and overall survival of patients (Zhu et al, 2015;Chen et al, 2018;Chen et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, the role of lncRNAs in osteosarcoma pathogenesis has attracted much attention and is being heavily investigated, particularly through high-throughput sequencing. Several of these lncRNAs are implicated in the downregulation of target gene expression (Yang et al, 2019), while others have been found to upregulate the expression of target genes (Li et al, 2013;Deng et al, 2019). An increasing number of studies indicate that lncRNAs play an important role in osteosarcoma development by affecting the following processes: cell proliferation, cellular invasion, migration, metastasis, stemness, fate, and EMT (Huang et al, 2018;Shen et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…A mechanism of interest, which has been reported on several times, involves lncRNAs working as competing endogenous RNAs (ceRNA), in which the lncRNA can act as a sponge for specific miRNAs and indirectly regulate the expression of tumorrelated genes Deng et al, 2019;Shen et al, 2019). Tp53, a well-known and extensively studied gene in tumors, was first reported to exhibit intron 1 rearrangement (Masuda et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

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LncRNA LINC00588 Suppresses the Progression of Osteosarcoma by Acting as a ceRNA for miRNA-1972

et al. 2020

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Long non-coding RNAs (lncRNAs) are being found to play an increasingly important role in the development of tumors. However, their biological functions and the underlying mechanisms remain unclear. Using information from GEO Datasets, we found that the lncRNA LINC00588 was downregulated in osteosarcoma (OS) in bone but was upregulated in the metastatic tumor present in the lung. We assessed the function of LINC00588 using both overexpression and knockout studies. We performed colony formation assay, CCK-8 assay, flow cytometry, wound healing assay, transwell assay, and RT-qPCR assay and used a xenograft model to investigate the influence of LINC00588 on cell proliferation, viability, cell apoptosis and cycle, migration, invasion, endothelial cell function, EMT (epithelial to mesenchymal transition), and tumor growth, respectively. Overexpression of LINC00588 appeared to inhibit cell proliferation, viability, migration, invasion, endothelial cell function, EMT, and tumor growth but not apoptosis, while we got the opposite result when we knocked down LINC00588. Next, we predicted that LINC00588 bound to miRNA-1972 and significantly downregulated its expression, which we then verified through a luciferase reporter assay. Subsequently, we knocked down miR1972 and performed CCK-8 and transwell assays to demonstrate that downregulation of miRNA-1972 could substantially inhibit the viability and invasion of osteosarcoma cells. The expression of TP53 was downregulated at the protein level but not at the mRNA level after the overexpression of miRNA-1972. Taken together, our findings indicate that LINC00588 plays a role in OS development by downregulating the expression of miRNA-1972, which can, in turn, inhibit the expression of TP53. Hence, we believe that the LINC00588/miRNA-1072/TP53 axis could potentially serve as a therapeutic target or diagnostic biomarker for osteosarcoma.

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“…OS is a common aggressive mesenchyme-derived bone tumor ranked among the top causes of cancer-related death in the pediatric populations [27]. The cancer's large tumor heterogeneity and its low prevalence make it tough to gain meaningful progress in patient's survival [28].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1 aggravates osteosarcoma carcinogenesis via regulating the microRNA-579/MMP13 axis

Wang

Zhou

Zhang

et al. 2020

Preprint

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Background: Previous studies have suggested that long non-coding RNAs (lncRNAs) were involved in tumorigenesis in various human carcinomas, including osteosarcoma (OS). However, the expression and specific role of lncRNA NEAT1 in OS remain unknown. The current study aimed at revealing the role of lncRNA NEAT1 and its related mechanism in OS.Methods: Expression profiles of lncRNAs in OS tissues were constructed, and lncRNA NEAT1 expression was verified with RT-qPCR followed by sub-localization. LncRNA-microRNA (miRNA) and miRNA-mRNA interactions were predicted. Validation was performed using dual luciferase reporter gene assay, and gain-and loss-of-function experiments. The effects of lncRNA NEAT1, miR-579 and MMP13 on the proliferation, migration and invasion, epithelial-mesenchymal transition (EMT) of OS cells were detected using colony formation, cell counting kit-8 (CCK-8), Transwell assays and Western blot analysis. Results: LncRNA NEAT1 overexpression was observed in OS tissues and cell lines which located in the cytoplasm. Transfection-induced downregulation of lncRNA NEAT1/MMP13 or overexpression of miR-579 blocked the progression of OS cells. LncRNA NEAT1 promotes MMP13 through sponging miR-579.Conclusion: LncRNA NEAT1 might be beneficial for OS aggravation via sponging miR-579 and facilitating MMP13 expression, which represents a candidate marker and target for OS therapy.clarify the invisible mechanism underlying tumorigenesis and to develop novel molecular targets of OS.Long non-coding RNAs (lncRNAs), surpassing over 200 nucleotides in length, are a prominent class of RNAs exerting a crucial regulatory potential in tumor cell behaviors [6]. Increasing evidence has illustrated that aberrantly expressed lncRNAs were highly associated with the occurrence and development of many human malignancies, including OS [7-9]. Nuclear enriched abundant transcript 1 (NEAT1) is a lncRNA transcribed from the diverse endocrinal neoplasia locus [10]. The interaction of lncRNA NEAT1 has been documented in glioma, prostate cancer and lung adenocarcinoma [11][12][13].LncRNA NEAT1 was also suggested as a tumor promotor in OS by several studies [14][15][16].MicroRNAs (miRNAs) are tiny (~ 22 nucleotides) endogenous non-coding RNA molecules which act at the post-transcriptional level and regulate mRNA expression [17]. They are involved in multiple complicated cellular behaviors [18]. Importantly, emerging evidence has pointed out that miRNAs participate in OS, such as miR-18a-5p, miR-671-5p, miR-1301, and miR-212 [19-22]. MiR-579 was reported to be associated with malignancies, such as breast cancer, ovarian cancer, and human glioblastoma [23][24][25]. However, its function in OS deserves further studies.LncRNAs are proved to serve as competing endogenous RNAs (ceRNAs), which sponges certain miRNAs to mediate its target gene, thus changing the post-transcriptional regulation [1]. However, the concrete influence that lncRNA NEAT1 and miR-579 exerts on OS, especially their interaction is still to be elucidated. In this experimen...

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lncRNA SNHG1 negatively regulates miRNA‑101‑3p to enhance the expression of ROCK1 and promote cell�proliferation, migration and invasion in osteosarcoma

Cited by 40 publications

References 39 publications

Biology and pathogenesis of human osteosarcoma (Review)

Biology and pathogenesis of human osteosarcoma (Review)

LncRNA LINC00588 Suppresses the Progression of Osteosarcoma by Acting as a ceRNA for miRNA-1972

Long noncoding RNA NEAT1 aggravates osteosarcoma carcinogenesis via regulating the microRNA-579/MMP13 axis

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