tae226 has been researched along with Mouth-Neoplasms* in 2 studies
2 other study(ies) available for tae226 and Mouth-Neoplasms
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[Effect of the focal adhesion kinase inhibitor TAE226 on the epithelial-mesenchymal transition in human oral squamous cell carcinoma cell line].
To study the effect of the focal adhesion kinase inhibitor TAE226 on epithelial-mesenchymal transition (EMT) in human oral squamous cell carcinoma (OSCC) cell line.. HSC-3 and HSC-4 cells were cultured with TAE226 under different concentrations (0, 1, 5, and 10 μmol·L⁻¹) for 24, 48, and 72 h. Real-time quantitative polymerase chain reaction was performed to detect the mRNA expressions of E-cadherin and Vimentin. The protein expressions of E-cadherin and Vimentin were determined by Western blot assay after 48 h of TAE226 treatment.. Real-time quantitative polymerase chain reaction showed that increasing the TAE226 dose and reaction time resulted in increased and decreased E-cadherin and Vimentin mRNA expressions, respectively (P<0.05). Western blot assays showed that increasing the TAE226 dose resulted in increased and decreased E-cadherin and Vimentin protein expressions, respectively (P<0.05).. TAE226, which is expected to be an effective drug for OSCC treatment, can effectively inhibit the EMT of the OSCC cell line.. 目的 探究黏着斑激酶抑制剂TAE226对人口腔鳞状细胞癌细胞上皮间质转化(EMT)过程的影响。方法 不同浓度(0、1、5、10 μmol·L⁻¹)的TAE226作用于人口腔鳞状细胞癌HSC-3和HSC-4细胞24、48、72 h后,实时定量聚合酶链反应检测EMT标志物E-钙黏蛋白(E-cadherin)、波形蛋白(Vimentin)的mRNA表达;蛋白质印迹法检测E-cadherin、Vimentin在TAE226作用48 h后的蛋白表达。结果 实时定量聚合酶链反应检测表明,随着TAE226作用时间和浓度的增加,E-cadherin mRNA的表达增加,Vimentin mRNA的表达降低(P<0.05)。蛋白质印迹法检测表明,随着TAE226浓度的增加,E-cadherin蛋白的表达增加,Vimentin蛋白的表达降低(P<0.05)。结论 TAE226能有效抑制人口腔鳞状细胞癌细胞株的EMT进程,有望成为治疗口腔鳞状细胞癌的有效药物之一。. Topics: Cadherins; Carcinoma, Squamous Cell; Cell Line, Tumor; Epithelial-Mesenchymal Transition; Focal Adhesion Protein-Tyrosine Kinases; Humans; Morpholines; Mouth Neoplasms; Vimentin | 2020 |
Anti-tumor effect of a novel FAK inhibitor TAE226 against human oral squamous cell carcinoma.
Focal adhesion kinase (FAK) overexpression is frequently found in invasive and metastatic cancers, but its role in oral squamous cell carcinoma is not yet well understood. In order to seek therapies targeting oral squamous cell carcinoma, we developed the novel FAK Tyr(397) inhibitor TAE226 and investigated its anti-tumor effects and mechanisms.. Expression of phosphorylated FAK Tyr(397) was examined by immunohistochemical and immunoblot analysis. The effect of TAE226 on in vitro and in vivo studies were confirmed by proliferation, cell cycle, apoptosis and angiogenesis analysis.. We found that phosphorylated FAK was highly expressed in human tongue oral squamous cell carcinoma in patients. Importantly, TAE226 greatly suppressed the proliferation, migration and invasion of human oral squamous cell carcinoma SAS cells with an apparent structural change of actin fiber and a loss of cell adhesion. In addition, TAE226 inhibited the expression of phospho-FAK Tyr(397) and phospho AKT Ser(473), resulting in caspase-mediated apoptosis. Furthermore, oral administration of TAE226 in mice suppressed the growth and angiogenesis of oral squamous cell carcinoma xenografts in vivo.. Our results provide compelling evidence that FAK is critically involved in oral squamous cell carcinoma and that the FAK inhibitor TAE226 can potentially be effectively used for the treatment of oral squamous cell carcinoma. Topics: Animals; Apoptosis; Carcinoma, Squamous Cell; Cell Cycle; Cell Proliferation; Cell Transformation, Neoplastic; Female; Focal Adhesion Protein-Tyrosine Kinases; Humans; Mice; Mice, Inbred BALB C; Mice, Nude; Morpholines; Mouth Neoplasms; Phosphorylation; Proto-Oncogene Proteins c-akt | 2012 |