Receptor for advanced glycation end-products (RAGE) is overexpressed in human osteosarcoma and promotes the proliferation of osteosarcoma U-2OS cells in vitro

Zhang, Q; Jin, Yongfeng; Cf, Zhao; Wang, WJ; Gy, Liu

doi:10.4238/gmr.15027817

Cited by 11 publications

(12 citation statements)

References 17 publications

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“…Therefore, growth factors, such as transforming growth factor (TGF), are deemed to be involved in the pathogenesis of OS due to the acceleration of OS cell proliferation and oncogenesis [Zhang, 2016]. A study has reported TGF-b1 could induce epithelial to mesenchymal transition (EMT) in lung cancer cells [Jo et al, 2015].…”

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confidence: 99%

Retracted: MicroRNA‐126 Inhibits Proliferation, Migration, Invasion, and EMT in Osteosarcoma by Targeting ZEB1

Jiang

Zhang

Liu

et al. 2017

J of Cellular Biochemistry

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Osteosarcoma (OS) is a tumor with rapid progression, high metastatic potential and poor clinical prognosis. This study was aimed to investigate the function of miR-126 in OS cells. The miR-126 expression in OS cell lines and OS tissues were explored by qRT-PCR. Then, the effects of miR-126 on proliferation, cycle, migration, invasion, and transforming growth factor (TGF)-β1 induced epithelial to mesenchymal transition (EMT) were assessed. Predicted by TargetScan, one of target genes for miR-126 was verified by luciferase activity assay. Meantime, the mRNA and protein expressions of ZEB1 were assessed by qRT-PCR and Western blot assay. Subsequently, the effect of ZEB1 silence on miR-126 down-regulated cells was also evaluated. Finally, the expressions of key kinases involved in c-Jun N-terminal kinase (JNK) and Janus-activated kinase (JAK)-1/signal transducer and activator of transcription (STAT)-3 pathways were detected by Western blot analysis. Result showed that miR-126 was down-regulated in OS tissues and cell lines. Overexpression of miR-126 significantly inhibited cell proliferation, migration, invasion, and TGF-β1 induced EMT. The effect of miR-126 knockdown was just the opposite. ZEB1 was predicted and verified as a target gene of miR-126. Meantime, the influence of miR-126 knockdown was abrogated by ZEB1 silence. Additionally, the phosphorylation levels of c-Jun, JNK, JAK1, and STAT3 were down-regulated in miR-126 over-expressed cells, and the effect of miR-126 knockdown was reversed by ZEB1 silence. In conclusion, miR-126 inhibits proliferation, migration, invasion and EMT in OS by targeting ZEB1 through inactivation of JNK and JAK1/STAT3 pathways. J. Cell. Biochem. 118: 3765-3774, 2017. © 2017 Wiley Periodicals, Inc.

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confidence: 99%

Retracted: MicroRNA‐126 Inhibits Proliferation, Migration, Invasion, and EMT in Osteosarcoma by Targeting ZEB1

Jiang

Zhang

Liu

et al. 2017

J of Cellular Biochemistry

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“…1 Clinical data display that OS occurs widely in children or teenagers under the 20 years of age. 1 Clinical data display that OS occurs widely in children or teenagers under the 20 years of age.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Inositol polyphosphate‐4‐phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3‐kinase/protein kinase B pathway

Dong

Yang

et al. 2018

J of Cellular Biochemistry

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Osteosarcoma (OS) is an aggressive malignant tumor of bone, which often occurs in children and adolescents. Currently, the effective method for the treatment of OS is still limited. The study aimed to investigate the synergistic antitumor effect of inositol polyphosphate-4-phosphatase, type-II (INPP4B) and rucaparib on OS cells. The expression levels of INPP4B in OS tissues and OS cell lines were examined by quantitative real-time polymerase chain reaction and Western blot analysis. SaOS2 and U2OS cells were then transfected with overexpression vector of INPP4B or were treated with different concentrations of rucaparib, and cell viability, cell cycle, and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry. Western blot assay uncovered the combined effects of INPP4B and rucaparib on cell cycle, apoptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signal pathway. Further, the tumor formation was examined in vivo. Results showed that INPP4B was low expressed in OS tissues and in OS cell lines. INPP4B overexpression significantly decreased cell viability and induced apoptosis in SaOS2 and U2OS cells. Additionally, rucaparib remarkably reduced cell viability in a dose-dependent and time-dependent manner. Meanwhile, rucaparib suppressed cell cycle progression in the S phase and promoted apoptosis in a dose-dependent manner. Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells. Finally, combination of INPP4B overexpression and rucaparib inhibited tumor formation in vivo. The study demonstrated that INPP4B and rucaparib exhibited synergistic antitumor effect by regulating PI3K/AKT pathway in OS cells.

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“…Local invasion and metastasis are the primary reasons for death in osteosarcoma patients [7]. Previous studies have suggested that osteosarcoma was relative higher in metastasis, with 80% of the metastases occurring in lung and the others in bone and lymph nodes [19]. Nowadays, one of the most prevalent therapies for osteosarcoma is pre-and post-operational chemotherapy combined with surgical treatment.…”

Section: Discussionmentioning

confidence: 99%

MicroR-542-3p can mediate ILK and further inhibit cell proliferation, migration and invasion in osteosarcoma cells

Cai

Zuo

2019

Aging

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MiR-542-3p and its target gene integrin linked kinase (ILK) in human osteosarcoma together with the differentially expressed genes from osteosarcoma tissues was analyzed through bioinformatics analysis in this study. Real time quantitative polymerase chain reaction (qRT-PCR) and western blot showed that the miR-542-3p expression decreased while the ILK expression increased in the osteosarcoma tissues. The overexpressed miR-542-3p or silenced ILK restrained cell invasion, proliferation and migration and arrested cell cycle, facilitated cell apoptosis in U-2OS and 143B cells. The dual-luciferase assay confirmed the targeting relationship between miR-542-3p and ILK. MiR-542-3p overexpression inhibited osteosarcoma growth in vivo. In conclusion, miR-542-3p overexpression down-regulated its target gene ILK, promoted osteosarcoma cells apoptosis and inhibited their proliferation, migration and invasion.

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Receptor for advanced glycation end-products (RAGE) is overexpressed in human osteosarcoma and promotes the proliferation of osteosarcoma U-2OS cells in vitro

Cited by 11 publications

References 17 publications

Retracted: MicroRNA‐126 Inhibits Proliferation, Migration, Invasion, and EMT in Osteosarcoma by Targeting ZEB1

Retracted: MicroRNA‐126 Inhibits Proliferation, Migration, Invasion, and EMT in Osteosarcoma by Targeting ZEB1

Retracted: Inositol polyphosphate‐4‐phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3‐kinase/protein kinase B pathway

MicroR-542-3p can mediate ILK and further inhibit cell proliferation, migration and invasion in osteosarcoma cells

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