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Twist1调控上皮-间质转化促进舌鳞癌细胞顺铂耐药机制的研究 被引量:2

Study on Twist1 promoting epithelial-mesenchymal transition and drug-resistance in tongue squamous cell carcinoma
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摘要 目的 :探讨Twist1调控上皮-间质转化(EMT)促进舌鳞状细胞癌细胞顺铂耐药的机制。方法 :在CAL27/CDDP中转染Twist1 siRNA,免疫印迹及免疫荧光检测E-cadherin、Vimentin的表达;免疫印迹检测Twist1、Slug的表达;Transwell及划痕实验检测细胞的侵袭、迁移能力;MTT检测细胞对顺铂的半抑制率。采用SPSS17.0软件包对结果进行单因素方差分析。结果:转染Twist1 siRNA可逆转CAL27/CDDP的EMT表型,E-cadherin表达增强,Vimentin、Twist1及Slug表达降低,细胞的侵袭、迁移能力明显降低,IC_(50)下降41.75%±5.10%(P<0.01)。结论:Twist1可通过调控上皮-间质转化而促进舌鳞癌细胞的顺铂耐药。 URPOSE: The aim of this study was to investigate the mechanism of Twist1 regulating epithelial-mesenchymal transition (EMT) and cisplatin-resistance in tongue squamous carcinoma cells. METHODS: TSCC CDDP resistant cell line CAL27/CDDP was transfected with Twist1 siRNA. Western blot and immunofluorescence staining were used to detect the expression of E-cadherin and Vimentin; Western blot was used to detect the expression of Twist1 and Slug; Transwell assay and scratch test were used to detect the invasion and migration capabilities; MTT was used to analyze the half maximal inhibitory concentration (IC50) values. One-way ANOVA was used to analyze the results with SPSS 17.0 software package. RESULTS: Twist1 siRNA transfection reversed EMT phenotype of CAL27/CDDP. The expression of E-cadherin was up-regulated and the expression of Vimentin, Twist1 and Slug was down-regulated. The motility was significantly decreased. The IC50 of CAL27/CDDP decreased by 41.75%±5.10%(P〈0.01). CONCLUSIONS: Twist1 promotes EMT and CDDP drug-resistance in TSCC.
出处 《中国口腔颌面外科杂志》 CAS 2018年第1期1-5,共5页 China Journal of Oral and Maxillofacial Surgery
基金 国家自然科学基金(81502350) 广东省自然基础与应用基础研究专项(广东省自然科学基金)自由申请项目(2016A030313352)
关键词 舌鳞状细胞癌 上皮-间质转化 TWIST1 耐药性 Tongue squamous cell carcinoma Epithelial-mesenchymal transition Twist1 Drug resistance
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  • 1Jianguo Song.EMT or apoptosis: a decision for TGF-β[J].Cell Research,2007,17(4):289-290. 被引量:9
  • 2Bernier J,Cooper JS. Chemoradiation after surgery for high-riskhead and neck cancer patients: how strong is the evidence?[J].Oncologist, 2005,10(3):215-224.
  • 3Kajiyama H, Shibata K, Terauchi M, et al. Chemoresistance topaclitaxel induces epithelial-mesenchymal transition andenhances metastatic potential for epithelial ovarian carcinomacells[J]. Int J Oncol, 2007,31(2) :277-283.
  • 4Thomson S,Buck E,Petti F,et al. Epithelial to mesenchymaltransition is a determinant of sensitivity of non-small-cell lungcarcinoma cell lines and xenografts to epidermal growth factorreceptor inhibition[J]. Cancer Res, 2005,65(20) ;9455-9462.
  • 5Yauch RL, Januario T, Eberhard DA, et al. Epithelial versusmesenchymal phenotype determines in vitro sensitivity andpredicts clinical activity of erlotinib in lung cancer patients [J].Clin Cancer Res, 2005,11(24 Pt 1) ;8686-8698.
  • 6Yang AD, Fan F, Camp ER, et al. Chronic oxaliplatinresistance induces epithelial-to-mesenchymal transition incolorectal cancer cell lines [J]. Clin Cancer Res, 2006,12( 14Pt 1)..4147-4153.
  • 7Sabbah M, Emami S, Redeuilh G, et al. Molecular signatureand therapeutic perspective of the epithelial-to-mesenchymaltransitions in epithelial cancers [J]. Drug Resist Updat, 2008,11(4-5):123-151.
  • 8Fuchs BC, Fujii T,Dorfman JD, et al. Epithelial-to-mesenchymal transition and integrin-linked kinase mediatesensitivity to epidermal growth factor receptor inhibition inhuman hepatoma cells [J]. Cancer Res, 2008,68 (7) :2391-2399.
  • 9Takebe N, Warren RQ, Ivy SP. Breast cancer growth andmetastasis : interplay between cancer stem cells, embryonicsignaling pathways and epithelial-to-mesenchymal transition [J].Breast Cancer Res, 2011,13(3):211.
  • 10Krawczyk N,Meier-Stiegen F, Banys M, et al. Expression ofstem cell and epithelial-mesenchymal transition markers incirculating tumor cells of breast cancer patients[J]. Biomed ResInt, 2014:415721.

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