Abstract
Abstract Transforming acidic coiled-coil protein 3 (TACC3) is a member of TACC family, essential for the maintenance of centrosome integrity and the regulation of microtubule assembly and spindle stability during mitosis. In addition to its function in mitosis, TACC3 has been shown to be involved in controlling cell growth, differentiation and transcriptional regulation. Interestingly, deregulated expression of TACC3 has been found in many human cancers, including breast, ovary, bladder, glioblastoma and non-small cell lung cancer. Moreover, our previous microarray analysis suggested that overexpression of TACC3 may be associated with the progression, metastasis and chemoresistance of cervical cancer. Although these findings indicate that TACC3 may play an important role in human cancer, the fundamental molecular mechanisms underlying how TACC3 contributes to cancer initiation, progression and metastasis, and its clinical significance remain elusive. Here, we explored the significance of TACC3 in cervical cancer. Using cervical cancer tissue microarrays, we found that TACC3 is overexpressed in cervical cancer compared with normal cervix. By modulating the expression of TACC3, we found that overexpression of TACC3 leads to changes in cell morphology, proliferation, transforming capability, migratory/invasive behavior as well as the expression of epithelial-mesenchymal transition (EMT)-related markers. Moreover, phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated protein kinases (ERKs) signaling pathways are critical for TACC3-mediated EMT process. Notably, depletion of TACC3 is sufficient to suppress EMT phenotype. Our findings, therefore, identify a novel mechanism that promotes EMT, possibly leading to a more malignant and metastatic tumor phenotype as well as a potential biomarker for diagnosis, prognosis and therapy for cervical cancer. Citation Format: Geun-Hyoung Ha, Jong-Sup Park, Eun-Kyoung Y. Breuer. TACC3 promotes EMT through the up-regulation of PI3K/Akt and ERK signaling pathways. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4302. doi:10.1158/1538-7445.AM2013-4302
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