MicroRNA-100 inhibits osteosarcoma cell proliferation by targeting Cyr61

Huang, Jianhua; Gao, Kan-da; Lin, Jian; Wang, Qiugen

doi:10.1007/s13277-013-1146-8

Cited by 40 publications

(26 citation statements)

References 23 publications

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“…Because of the advancement of its treatment, including surgery and multi‐agent chemotherapy, the 5‐year survival rate in patients with primary osteosarcoma has improved over the past several decades 5, 6, 7, 8. However, the survival rate for this tumour remains low 9, 10, 11, 12.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

Shen

Chan

et al. 2016

J Cellular Molecular Medi

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Osteosarcoma is the most common primary bone tumour. Increasing evidence has demonstrated the pathogenic role of microRNA (miRNAs) dysregulation in tumour development. miR‐379 was previously reported to function as an oncogenic or tumour‐suppressing miRNA in a tissue‐dependent manner. However, its function in osteosarcoma remains unknown. In this study, we found that the expression of miR‐379 was downregulated in osteosarcoma tissues and cell lines. Further functional characterization revealed that miR‐379 suppressed osteosarcoma cell proliferation and invasion in vitro and retarded the growth of osteosarcoma xenografts in vivo. Mechanistically, PDK1 was identified as the direct target of miR‐379 in osteosarcoma, in which PDK1 expression was up‐regulated and showed inverse correlation with miR‐379. Enforced expression of PDK1 promoted osteosarcoma cell proliferation and rescued the anti‐proliferative effect of miR‐379. These data suggest that miR‐379 could function as a tumour‐suppressing miRNA via targeting PDK1 in osteosarcoma.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

Shen

Chan

et al. 2016

J Cellular Molecular Medi

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“…Previous studies have shown that miR-100 was significantly downregulated in osteosarcoma tissues and inhibited osteosarcoma cell proliferation by targeting Cyr61. 16 However, the role and mechanism of miR-100 in regulating tumorigenesis are still to be further elucidated. In this study, we will investigate (1) what is the role of miR-100 in osteosarcoma cell growth, migration, and invasion; (2) what is the direct target of miR-100 that is associated with cancer development; (3) whether there is a relationship between miR-100 and its direct target; and (4) whether miR-100 and its target are responsible for the resistance to cisplatin treatment in osteosarcoma.…”

Section: Introductionmentioning

confidence: 99%

MiR-100 Inhibits Osteosarcoma Cell Proliferation, Migration, and Invasion and Enhances Chemosensitivity by Targeting IGFIR

Liu

Zhu

Wang

et al. 2016

Technol Cancer Res Treat

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MicroRNAs are highly conserved noncoding RNA that negatively modulate protein expression at a posttranscriptional and/or translational level. MicroRNAs play an important role in the development and progression of human cancers, including osteosarcoma. Recent studies have shown that miR-100 was downregulated in many cancers; however, the role of miR-100 in human osteosarcoma has not been totally elucidated. In this study, we demonstrate that the expression of miR-100 was significantly downregulated in human osteosarcoma tissues compared to the adjacent tissues. Enforced expression of miR-100 inhibited cell proliferation, migration, and invasion abilities of osteosarcoma cells, U-2OS, and MG-63. Additionally, miR-100 also sensitized osteosarcoma cells to cisplatin and promoted apoptosis. Furthermore, overexpression of miR-100 decreased the expression of insulin-like growth factor I receptor and inhibited PI3K/AKT and MAPK/ERK signaling. In human clinical specimens, insulin-like growth factor I receptor was inversely correlated with miR-100 in osteosarcoma tissues. Collectively, our results demonstrate that miR-100 is a tumor suppressor microRNA and indicate its potential application for the treatment of osteosarcoma in future.

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“…Moreover, the expression of the CYR61 gene is regulated by TP53, miRNA-22 and miRNA-100 as well as through activation of the PI3K/Akt signaling [10,18,19]. It is interesting to note that degradome products of this matricellular protein may modulate the pathological angiogenesis in the retina [20].…”

Section: Experimental Researchmentioning

confidence: 99%

“…Adipose tissue growth is a center of obesity, is tightly associated with apoptosis and the cell proliferation processes, and is controlled by different interconnected regulatory factors and enzymes [1,6,8]. Special interest should be given to key regulatory factors and enzymes, which control cell growth and survival, especially GADD45A, PLAGL1, CYR61, PPP1R15A, TFPI2, HSPA6, and ITGA5 [10][11][12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

“…The cysteine-rich angiogenic inducer 61 (CYR61), also known as CCN family member 1 and insulin-like growth factor-binding protein 10 (IGFBP10), is a secreted, cysteinerich, heparin-binding protein encoded by a growth factorinducible, immediate-early gene and acting as an extracellular, matrix-associated signaling molecule, which promotes matrix remodeling, cell proliferation, cell migration and adhesion by up-regulating the expression of a number of genes [10][11][12]. …”

Section: Introductionmentioning

confidence: 99%

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Expression of Endoplasmic Reticulum Stress Related Genes in Blood Cells of Obese Boys with and without Insulin Resistance

Minchenko¹

2015

Int J Biomed

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Objective: to study the changes in the expression level of the subset of genes, encoding for important cell growth factors and enzymes, which play an important role in the control of cellular growth and apoptosis, in blood cells of obese boys with and without insulin resistance for evaluation of its possible significance in the development of obesity and impaired insulin sensitivity. Material and Methods:We studied the expression of genes, which are responsible for control of cell growth and survival, in blood cells of obese boys with normal and impaired insulin sensitivity as compared to normal (control) individuals.Results: It was shown that the expression level of PLAGL, CYR61, ITGA5, and TFPI2 genes is increased, but the GADD45A gene is decreased in blood cells of obese children with normal insulin sensitivity as compared to the control group. Insulin resistance in obese boys leads to the up-regulation of PPP1R15A and PLAGL1 gene expressions as well as to the down-regulation of TFPI2, GADD45A, ALDH1A2, CYR61, and HSPA6 genes in blood cells as compared to obese patients with normal insulin sensitivity.Conclusion: Results of this study provide evidence that obesity affects the expression of the subset of genes related to the control of cell growth and survival in blood cells and that impaired insulin sensitivity in obesity is associated with changes in the expression level of PLAGL, CYR61, GADD45A, PPP1R15A, TFPI2, ALDH1A2, and HSPA6 genes, which possibly contributes to the development of obesity and its metabolic complications, including insulin resistance.

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MicroRNA-100 inhibits osteosarcoma cell proliferation by targeting Cyr61

Cited by 40 publications

References 23 publications

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

MiR-100 Inhibits Osteosarcoma Cell Proliferation, Migration, and Invasion and Enhances Chemosensitivity by Targeting IGFIR

Expression of Endoplasmic Reticulum Stress Related Genes in Blood Cells of Obese Boys with and without Insulin Resistance

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