miR-22 inhibits osteosarcoma cell proliferation and migration by targeting HMGB1 and inhibiting HMGB1-mediated autophagy

Guo, Sisi; Bai, Rui; Liu, Wanlin; Zhao, Aiqing; Zhao, Zhenqun; Wang, Yuxin; Wang, Yong; Zhao, Wei; Wang, Wenxuan

doi:10.1007/s13277-014-1965-2

Cited by 68 publications

(53 citation statements)

References 39 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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“…Recent studies have demonstrated that HMGB1 is an important regulator of autophagy and that HMGB1-regulated autophagy is a significant contributor to drug resistance following treatment with cytotoxic agents in tumor cells32344748. In the present study, we found that OMT increased the expression of HMGB1 in a dose- and time-dependent manner.…”

Section: Discussionsupporting

confidence: 70%

HMGB1-mediated autophagy decreases sensitivity to oxymatrine in SW982 human synovial sarcoma cells

Cai

Liu

et al. 2016

Sci Rep

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Oxymatrine (OMT) is a type of alkaloid extracted from a traditional Chinese medicinal herb, Sophora flavescens. Although the antitumor activities of OMT have been observed in various cancers, there are no reports regarding the effects of OMT on human synovial sarcoma. In the present study, we analyzed the antitumor activities of OMT in SW982 human synovial sarcoma cells and determine whether high mobility group box protein 1 (HMGB1)-mediated autophagy was associated with its therapeutic effects. We found that OMT exhibited antitumor activity in SW982 cells and facilitated increases in autophagy. Inhibition of autophagy by 3-MA or ATG7 siRNA increased the level of apoptosis, which indicated that OMT-induced autophagy protected cells from the cytotoxicity of OMT. Administration of OMT to SW982 cells increased the expression of HMGB1. When HMGB1 was inhibited via HMGB1-siRNA, OMT-induced autophagy was decreased, and apoptosis was increased. Furthermore, we found that HMGB1-siRNA significantly increased the expression of p-Akt and p-mTOR. OMT-induced autophagy may be mediated by the Akt/mTOR pathway, and HMGB1 plays a vital role in the regulation of autophagy. Therefore, we believe that combining OMT with an inhibitor of autophagy or HMGB1 may make OMT more effective in the treatment of human synovial sarcoma.

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“…However, possibly as a compensatory effect, miR-22 was also upregulated during chemotherapy; and overexpressed miR-22 targeted the 3′UTR of HMGB1 and inhibited HMGB1-promoted autophagy [102]. Additionally, miR-22 inhibited osteosarcoma cell proliferation and migration by targeting HMGB1 and inhibiting HMGB1-mediated autophagy [103]. The upregulated HMGB1 increased the formation of the Beclin1-PtdIns3KC3 complex and stimulated autophagosome maturation and autophagy by competing with Bcl-2 to bind Beclin1.…”

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Yang

et al. 2016

Oncotarget

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Osteosarcoma is the most common primary bone tumor in children and adolescents. Although combined therapy including surgery and multi-agent chemotherapy have resulted in great improvements in the overall survival of patients, chemoresistance remains an obstacle for the treatment of osteosarcoma. Molecular targets or effective agents that are actively involved in cell death including apoptosis, autophagy and necroptosis have been studied. We summarized how these agents (novel compounds, miRNAs, or proteins) regulate apoptotic, autophagic and necroptotic pathways; and discussed the current knowledge on the role of these new agents in chemotherapy resistance in osteosarcoma.

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miR-22 inhibits osteosarcoma cell proliferation and migration by targeting HMGB1 and inhibiting HMGB1-mediated autophagy

Cited by 68 publications

References 39 publications

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

RETRACTED: MicroRNA‐379 suppresses osteosarcoma progression by targeting PDK1

HMGB1-mediated autophagy decreases sensitivity to oxymatrine in SW982 human synovial sarcoma cells

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

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