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MALAT1-miR-101-SOX9 feedback loop modulates the chemo-resistance of lung cancer cell to DDP via Wnt signaling pathway.MALAT1- miR-101- SOX9反馈环通过Wnt信号通路调节肺癌细胞对顺铂的化疗耐药性。
Oncotarget. 2017 Oct 9;8(55):94317-94329. doi: 10.18632/oncotarget.21693. eCollection 2017 Nov 7.
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Interplay between Notch1 and Notch3 promotes EMT and tumor initiation in squamous cell carcinoma.Notch1 和 Notch3 之间的相互作用促进鳞状细胞癌中的 EMT 和肿瘤起始。
Nat Commun. 2017 Nov 24;8(1):1758. doi: 10.1038/s41467-017-01500-9.
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miR-592 functions as a tumor suppressor in human non-small cell lung cancer by targeting SOX9.miR-592通过靶向SOX9在人类非小细胞肺癌中发挥肿瘤抑制作用。
Oncol Rep. 2017 Jan;37(1):297-304. doi: 10.3892/or.2016.5275. Epub 2016 Nov 25.
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MicroRNA-101 inhibits proliferation, migration and invasion of human glioblastoma by targeting SOX9.微小RNA-101通过靶向SOX9抑制人胶质母细胞瘤的增殖、迁移和侵袭。
Oncotarget. 2017 Mar 21;8(12):19244-19254. doi: 10.18632/oncotarget.13706.
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E-cadherin re-expression shows in vivo evidence for mesenchymal to epithelial transition in clonal metastatic breast tumor cells.E-钙黏蛋白的重新表达显示了克隆性转移性乳腺癌细胞中从间充质到上皮转变的体内证据。
Oncotarget. 2016 Jul 12;7(28):43363-43375. doi: 10.18632/oncotarget.9715.
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Tumor Budding, EMT and Cancer Stem Cells in T1-2/N0 Oral Squamous Cell Carcinomas.T1-2/N0期口腔鳞状细胞癌中的肿瘤芽生、上皮-间质转化和癌症干细胞
Anticancer Res. 2015 Nov;35(11):6111-20.
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Bufalin Inhibits NCI-H460 Human Lung Cancer Cell Metastasis In Vitro by Inhibiting MAPKs, MMPs, and NF-κB Pathways.蟾毒灵通过抑制丝裂原活化蛋白激酶(MAPKs)、基质金属蛋白酶(MMPs)和核因子κB(NF-κB)信号通路在体外抑制NCI-H460人肺癌细胞转移。
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Correction: miR145 Targets the SOX9/ADAM17 Axis to Inhibit Tumor-Initiating Cells and IL6-Mediated Paracrine Effects in Head and Neck Cancer.更正:miR145靶向SOX9/ADAM17轴以抑制头颈癌中的肿瘤起始细胞和IL6介导的旁分泌效应。
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9
Decreased MT1-MMP in gastric cancer suppressed cell migration and invasion via regulating MMPs and EMT.胃癌中MT1-MMP的减少通过调节基质金属蛋白酶(MMPs)和上皮-间质转化(EMT)抑制细胞迁移和侵袭。
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10
SOX9 Overexpression Promotes Glioma Metastasis via Wnt/β-Catenin Signaling.SOX9过表达通过Wnt/β-连环蛋白信号通路促进胶质瘤转移。
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[性别决定区Y盒9下调对口腔鳞状癌细胞上皮间质转化及克隆的影响]

[Effect of down-regulation of sex determining region Y-box 9 on epithelial mesenchymal transition and cloning of oral squamous carcinoma cells].

作者信息

Yang Wen-Li, Sun Ming-Lei, Zhang Peng, Yu Wei-Wei, Zhou Hai-Xia, Sun Qiang

机构信息

Dept. of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

出版信息

Hua Xi Kou Qiang Yi Xue Za Zhi. 2019 Feb 1;37(1):13-18. doi: 10.7518/hxkq.2019.01.003.

DOI:10.7518/hxkq.2019.01.003
PMID:30854812
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7030727/
Abstract

OBJECTIVE

To investigate the effect of sex determining region Y-box 9 (SOX9) on epithelial mesenchymal transition (EMT) and cloning of oral squamous cell carcinoma (OSCC).

METHODS

siRNA control, SOX9 siRNA were transfected into BcaCD885 cells in OSCC. Simultaneously, cells that did not undergo transfection were used as the control. Quantitative real time polymerase chain reaction (qRT-PCR) and Western blot were used to select SOX9 siRNA1 with enhanced interference effect. A cell cloning assay was used to determine the cell's clone formation ability. E-cadherin and Vimentin expressions were detected by immunofluorescence. The expressions of E-cadherin, matrix metalloprotease 2 (MMP-2), Vimentin and matrix metalloprotease 9 (MMP-9) were detected by Western blot. Cell invasion and migration were detected in the Transwell compartment.

RESULTS

The levels of SOX9 mRNA and protein in SOX9 siRNA cells were significantly lower than those of the control (P<0.05). An increase in the number of SOX9 siRNA1 cell clonesled to the considerable decrease of the number of cell invasion and migration. In addition, levels of MMP-2 and MMP-9 proteins in cells decreased significantly compared with the control (P<0.05). The level of Vimentin expression in SOX9 siRNA1 cells decreased, and expression level of E-cadherin was elevated. Cell EMT was inhibited compared with the control, and the difference was statistically significant (P<0.05).

CONCLUSIONS

Down-regulation of SOX9 inhibited EMT, clonogenic formation, cell invasion and OSCC migration.

摘要

目的

探讨Y染色体性别决定区框9(SOX9)对口腔鳞状细胞癌(OSCC)上皮-间质转化(EMT)及克隆形成的影响。

方法

将siRNA对照、SOX9 siRNA转染至OSCC的BcaCD885细胞中。同时,将未进行转染的细胞作为对照。采用定量实时聚合酶链反应(qRT-PCR)和蛋白质免疫印迹法筛选干扰效果增强的SOX9 siRNA1。采用细胞克隆实验检测细胞的克隆形成能力。通过免疫荧光检测E-钙黏蛋白和波形蛋白的表达。采用蛋白质免疫印迹法检测E-钙黏蛋白、基质金属蛋白酶2(MMP-2)、波形蛋白和基质金属蛋白酶9(MMP-9)的表达。在Transwell小室中检测细胞侵袭和迁移情况。

结果

SOX9 siRNA细胞中SOX9 mRNA和蛋白水平显著低于对照组(P<0.05)。SOX9 siRNA1细胞克隆数量增加,导致细胞侵袭和迁移数量显著减少。此外,与对照组相比,细胞中MMP-2和MMP-9蛋白水平显著降低(P<0.05)。SOX9 siRNA1细胞中波形蛋白表达水平降低,E-钙黏蛋白表达水平升高。与对照组相比,细胞EMT受到抑制,差异具有统计学意义(P<0.05)。

结论

SOX9表达下调抑制EMT、克隆形成、细胞侵袭及OSCC迁移。