scholarly journals Overexpression of miR-422a inhibits cell proliferation and invasion, and enhances chemosensitivity in osteosarcoma cells

2016 ◽  
Vol 36 (6) ◽  
pp. 3371-3378 ◽  
Author(s):  
Mingjiang Liu ◽  
He Xiusheng ◽  
Xiangjun Xiao ◽  
Yichun Wang
Keyword(s):  
Cell Proliferation ◽  
Osteosarcoma Cells ◽  
Proliferation And Invasion

scholarly journals HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis

2020 ◽  
Vol 29 ◽  
pp. 096368972094844
Author(s):  
Jiankuo Guo ◽  
Dongmei Dou ◽  
Tianlun Zhang ◽  
Bo Wang
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Cisplatin Resistance ◽  
Transcriptional Level ◽  
Osteosarcoma Cells ◽  
Underlying Mechanisms ◽  
Lncrna Hotair ◽  
Proliferation And Invasion ◽  
Common Primary Malignant Bone ◽  
Huge Challenge

Osteosarcoma (OS) is a common primary malignant bone tumor among adolescences, and the emergence of multidrug resistance poses a huge challenge for clinical treatment of OS. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including OS. However, the underlying mechanisms of HOTAIR involved in drug resistance in OS are obscure. Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant OS tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance–related gene expression, cell proliferation, and invasion and promoted apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. Mechanism researches displayed that miR-106a-5p was downregulated in DDP-resistant OS tissues and cells. MiR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. Moreover, STAT3 was inhibited by miR-106a-5p at a post-transcriptional level, and the transfection of miR-106a-5p reversed the upregulation of STAT3 caused by HOTAIR overexpression. The increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion, and apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. What’s more, the transfection of STAT3 siRNA reversed the decrease of DDP resistance, cell proliferation, and invasion and rescued the increase of apoptosis induced by miR-106a-5p inhibition. These data suggested that HOTAIR enhanced DDP resistance of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/STAT3 axis.

scholarly journals Knockdown of KCNQ1OT1 Inhibits Proliferation, Invasion, and Drug Resistance by Regulating miR-129-5p-Mediated LARP1 in Osteosarcoma

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yunfei Zhang ◽  
Wei Cai ◽  
Yuli Zou ◽  
Hong Zhang
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Binding Activity ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Potential Mechanism ◽  
Osteosarcoma Cells ◽  
Rt Pcr ◽  
Transwell Assay ◽  
Proliferation And Invasion

KCNQ1OT1 exerts an important role in various cancers, but its role in osteosarcoma (OS) and the potential mechanism remain to be clarified. In the present research, we aimed to explore the effect of KCNQ1OT1 on osteosarcoma and further explore the special molecular mechanism. The expression of KCNQ1OT1 was analyzed in tumor and adjacent tissues of 30 patients with osteosarcoma by RT-PCR. Cell proliferation and invasion were explored using MTT and transwell assay, respectively. Luciferase reporter analysis and pull-down assay were performed to determine the binding activity of KCNQ1OT1 and miR-129-5p. The result revealed that KCNQ1OT1 was highly expressed in osteosarcoma tissues and cells. KCNQ1OT1-siRNA inhibited the proliferation, invasion, and drug resistance of osteosarcoma cells. The luciferase reporter assay and pull-down assay demonstrated that KCNQ1OT1 directly interact with miR-129-5p. In addition, miR-129-5p binds to LARP1 directly, and LARP1 promoted the proliferation, invasion, and drug resistance of osteosarcoma cells. What is more, KCNQ1OT1 promoted proliferation, invasion, and drug resistance via inhibiting the expression of miR-129-5p and further promoting the expression of miR-129-5p-mediated LARP1. Collectively, it suggests that downregulation of KCNQ1OT1 inhibits proliferation, invasion, and drug resistance by regulating miR-129-5p-mediated LARP1 in osteosarcoma cells.

scholarly journals The proliferation and invasion of osteosarcoma are inhibited by miR-101 via targetting ZEB2

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Haopeng Lin ◽  
Xiaodong Zheng ◽  
Ting Lu ◽  
Yang Gu ◽  
Canhao Zheng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Molecular Mechanisms ◽  
Bone Cell ◽  
Luciferase Reporter ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Direct Target ◽  
Proliferation And Invasion

AbstractHaving a better grasp of the molecular mechanisms underlying carcinogenesis and progression in osteosarcoma would be helpful to find novel therapeutic targets. Different types of cancers have presented abnormal expression of miRNA-101 (miR-101). Nevertheless, we still could not figure out what expression of miR-101 in human osteosarcoma is and its biological function. Thus, we conducted the present study to identify its expression, function, and molecular mechanism in osteosarcoma. We detected the expression of miR-101 in osteosarcoma samples and cell lines. The effects of miR-101 on osteosarcoma cells’ proliferation and invasion were evaluated. Luciferase reporter assay was applied to identify the direct target of miR-101. Compared with adjacent normal specimens and normal bone cell line by using qPCR, the expression levels of miR-101 in osteosarcoma specimens and human osteosarcoma cell lines distinctly decreased. According to function assays, we found that overexpression of miR-101 significantly inhibited the cell proliferation and invasion in osteosarcoma cells. Moreover, we confirmed that zinc finger E-box binding homeobox 2 (ZEB2) was a direct target of miR-101. In addition, overexpression of ZEB2 could rescue the inhibition effect of proliferation and invasion induced by miR-101 in osteosarcoma cells. MiR-101 has been proved to be down-regulated in osteosarcoma and has the ability to suppress osteosarcoma cell proliferation and invasion by directly targetting ZEB2.

scholarly journals LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway

2020 ◽  
Vol 29 ◽  
pp. 096368972095309
Author(s):  
Jianmin Liu ◽  
Ming Chen ◽  
Longyang Ma ◽  
Xingbo Dang ◽  
Gongliang Du
Keyword(s):  
Cell Proliferation ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Akt Pathway ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Luciferase Reporter Gene ◽  
Nude Mouse Model ◽  
Cell Functions ◽  
Proliferation And Invasion

Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.

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