miR-141-3p suppresses proliferation and promotes apoptosis by targeting GLI2 in osteosarcoma cells

Wang, Nan; Li, Pengcheng; Liu, Wei; Wang, Ningning; Lu, Zhi; Feng, Jianzhou; Zeng, Xiandong; Yang, Jiujie; Wang, Yong; Zhao, Wei

doi:10.3892/or.2017.6150

Cited by 25 publications

(25 citation statements)

References 37 publications

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“…The procedure was carried out as previously described . In briefly, HOS and 143B cells after different MALAT1, HDAC4, or miR‐140‐5p intervene were seeded on coverslips and incubated for 48 hours.…”

Section: Methodsmentioning

confidence: 99%

“…The procedure was carried out as previously described. 30 In briefly, HOS and 143B cells after different MALAT1, HDAC4, or miR-140-5p intervene were seeded on coverslips and incubated for 48 hours. All coverslips were fixed using of 4% paraformaldehyde for 30 minutes and then were permeabilized with 0.1% Triton X-100 for 2 minutes on ice.…”

Section: Terminal Deoxynucleotidyl Transferase (Tdt) Dutp Nick-end mentioning

confidence: 99%

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Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

Sun

Qin

2018

Cancer Medicine

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Noncoding RNAs regulate the initiation and progression of osteosarcoma (OS). The role of long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) playing in OS and whether the function it working out was achieved through HDAC4 pathway remain uncovered. In this study, we illustrated that MALAT1 was upregulated and was correlated with poor prognosis in OS patients. Meanwhile, we demonstrated that a depression of MALAT1 suppressed proliferation and promoted apoptosis in OS cell line HOS and 143B. Further, we verified that MALAT1 exerting its function via upregulating of histone deacetylase 4 (HDAC4). Through an online prediction, a series of luciferase assays and RNA pull‐down assays, we demonstrated that both MALAT1 and HDAC4 were the targets of microRNA‐140‐5p (miR‐140‐5p) via sharing a similar microRNA responding elements. Even further, we revealed that MALAT1 served as a ceRNA of HDAC4 via decoying of miR‐140‐5p. Finally, we proved that MALAT1 promoted OS tumor growth in an in vivo animal study. In summary, the outcomes of this study demonstrated the complex ceRNA network among MALAT, miR‐140‐5p, and HDAC4‐mediated proliferation and apoptosis in OS. This study might provide a new axial in molecular treatment of OS.

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Section: Methodsmentioning

confidence: 99%

Section: Terminal Deoxynucleotidyl Transferase (Tdt) Dutp Nick-end mentioning

confidence: 99%

Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

Sun

Qin

2018

Cancer Medicine

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“…30 miR-141-3p suppresses cell PLF and enhances APS by targeting GLI2 in osteosarcoma. 31 Importantly, miR-141-3p expression is down-regulated during the progression of GC, 32 expressing that miR-141-3p primarily exerts tumor-suppressive effect in GC. Accumulating researches reveal that lncRNAs work on miRNAs via serving as ceRNA and competitively inhibit miRNAs as molecular sponges.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer

et al. 2020

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Background Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. Methods RT‐PCR was used to detect HCG18 and miR‐141‐3p expression in GC specimen. GC cell lines (AGS and MKN‐28) were exploited as cell model. The biological effect of HCG18 on cancer cells was probed by CCK‐8, colony formation, flow cytometry, Transwell and wound‐healing experiments in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Interaction between HCG18 and miR‐141‐3p was determined by bioinformatics analysis, RT‐PCR, and luciferase reporter experiments. Downstream gene expression of miR‐141‐3p, including Wiskott–Aldrich syndrome protein interacting protein family member 1 (WIPF1), Yes associated protein 1 (YAP), and tafazzin (TAZ) were detected using Western blot. Results HCG18 was markedly up‐regulated in GC specimens, while miR‐141‐3p was markedly down‐regulated. Down‐regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR‐141‐3p transfection led to opposite effect. HCG18 could down‐regulate miR‐141‐3p through adsorbing it, and a negative association between HCG18 and miR‐141‐3p was found in GC specimens. HCG18 promoted WIPF1, YAP and TAZ expression, nonetheless, such influence was reversed by co‐transfecting with miR‐141‐3p. Conclusion HCG18 was aberrantly up‐regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR‐141‐3p expression.

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“…In addition, miR-141 was found to be overexpressed during senescence as a result of epigenetic regulation, which may lead to reduced tissue regeneration capacity and a decline in physiological functions 39 . Some studies have argued that downregulation of miR-141 could increase the proliferation of osteosarcoma cells and colorectal cancer SW480 cells 40,41 . In addition, it has been reported that upregulating miR-141-3p suppresses the invasion and migration of prostate cancer cells in vitro 42 .…”

Section: Discussionmentioning

confidence: 99%

Influence of MicroRNA‐141 on Inhibition of the Proliferation of Bone Marrow Mesenchymal Stem Cells in Steroid‐Induced Osteonecrosis via SOX11

Meng

Xue

Zhao

et al. 2020

Orthopaedic Surgery

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Objective To investigate whether miR‐141 and the sex determination region of Y chromosome box 11 (SOX11) play roles in steroid‐induced avascular necrosis of the femoral head (SANFH), and to explore whether miR‐141 could target SOX11 to influence the proliferation of bone marrow mesenchymal stem cells (BMSC). Methods Bone marrow mesenchymal stem cells (BMSC) were isolated and cultured from 4‐week‐old Sprague Dawley rats. A flow cytometry assay was performed to identify BMSC. BMSC were divided into two groups: a control group and a dexamethasone (DEX) group. BMSC were transfected by miR‐141 mimic, miR‐141 inhibitor, and SOX11. Real‐time polymerase chain reaction (PCR) assay was performed to investigate the mRNA expression of miR‐141 and SOX11. The results were used to determine the effect of transfection and to verify the expression in each group and the association between miR‐141 and SOX11. Luciferase reporter assay revealed the targeted binding site between miR‐141 and the 3′‐untranslated region of SOX11 mRNA. MTT assays were performed to investigate the proliferation of BMSC in the miR‐141 mimic, miR‐141 inhibitor, and SOX11 groups. Result The results of the flow cytometry assay suggested that cells were positive for CD29 and CD90 while negative for CD45. This meant that the isolated and cultured cells were not hematopoietic stem cells. In addition, cell transfection was successful based on the expression of miR‐141 and SOX11. According to the results of real‐time PCR assay, the mRNA expression of miR‐141 in SANFH was upregulated (4.117 ± 0.042 vs 1 ± 0.027, P < 0.001), while SOX11 was downregulated (0.611 ± 0.055 vs 1 ± 0.027, P < 0.001) compared with the control group. Based on the results of the luciferase experiment, MiR‐141 could directly target the expression of SOX11. Inhibition of miR‐141 could upregulate the expression of SOX11 (2.623 ± 0.220 vs 1 ± 0.095, P < 0.001) according to the results of a real‐time PCR assay. MiR‐141 inhibited the proliferation of BMSC (0.618 ± 0.092 vs 1.004 ± 0.082, P < 0.001), while suppression of miR‐141 increased the proliferation of BMSC (0.960 ± 0.095 vs 0.742 ± 0.091, P < 0.001). Furthermore, according to the results of the MTT assay, SOX11 promoted the proliferation of BMSC (1.064 ± 0.093 vs 0.747 ± 0.090, P < 0.001). Conclusion MiR‐141 inhibited the proliferation of BMSC in SANFH by targeting SOX11. Inhibition of miR‐141 upregulated the expression of SOX11 and promoted the proliferation of BMSC. MiR‐141 and SOX11 could be new targets for investigating the mechanism of SANFH.

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miR-141-3p suppresses proliferation and promotes apoptosis by targeting GLI2 in osteosarcoma cells

Cited by 25 publications

References 37 publications

Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

Long noncoding RNA MALAT1 regulates HDAC4‐mediated proliferation and apoptosis via decoying of miR‐140‐5p in osteosarcoma cells

Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer

Influence of MicroRNA‐141 on Inhibition of the Proliferation of Bone Marrow Mesenchymal Stem Cells in Steroid‐Induced Osteonecrosis via SOX11

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