TACC3 promotes epithelial-mesenchymal transition (EMT) through the activation of PI3K/Akt and ERK signaling pathways
- PMID: 23348690
- DOI: 10.1016/j.canlet.2013.01.013
TACC3 promotes epithelial-mesenchymal transition (EMT) through the activation of PI3K/Akt and ERK signaling pathways
Abstract
Transforming acidic coiled-coil protein 3 (TACC3) is a member of the TACC family, essential for mitotic spindle dynamics and centrosome integrity during mitosis. Mounting evidence suggests that deregulation of TACC3 is associated with various types of human cancer. However, the molecular mechanisms by which TACC3 contributes to the development of cancer remain largely unknown. Here, we propose a novel mechanism by which TACC3 regulates epithelial-mesenchymal transition (EMT). 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 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. Collectively, our findings identify TACC3 as a driver of tumorigenesis as well as an inducer of oncogenic EMT and highlight its overexpression as a potential therapeutic target for preventing EMT-associated tumor progression and invasion.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
Similar articles
-
Inactivation of M2 AChR/NF-κB signaling axis reverses epithelial-mesenchymal transition (EMT) and suppresses migration and invasion in non-small cell lung cancer (NSCLC).Oncotarget. 2015 Oct 6;6(30):29335-46. doi: 10.18632/oncotarget.5004. Oncotarget. 2015. PMID: 26336823 Free PMC article.
-
Consumption of high-fat diet induces tumor progression and epithelial-mesenchymal transition of colorectal cancer in a mouse xenograft model.J Nutr Biochem. 2012 Oct;23(10):1302-13. doi: 10.1016/j.jnutbio.2011.07.011. Epub 2012 Jan 4. J Nutr Biochem. 2012. PMID: 22221675
-
MiR-19a promotes epithelial-mesenchymal transition through PI3K/AKT pathway in gastric cancer.Int J Clin Exp Pathol. 2014 Sep 15;7(10):7286-96. eCollection 2014. Int J Clin Exp Pathol. 2014. PMID: 25400827 Free PMC article.
-
Epithelial-mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways.Oncogene. 2005 Nov 14;24(50):7443-54. doi: 10.1038/sj.onc.1209091. Oncogene. 2005. PMID: 16288291 Review.
-
A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition.Cell Adh Migr. 2015;9(4):317-24. doi: 10.1080/19336918.2015.1016686. Epub 2015 Aug 4. Cell Adh Migr. 2015. PMID: 26241004 Free PMC article. Review.
Cited by
-
ENKUR acts as a tumor suppressor in lung adenocarcinoma cells through PI3K/Akt and MAPK/ERK signaling pathways.J Cancer. 2019 Jul 5;10(17):3975-3984. doi: 10.7150/jca.30021. eCollection 2019. J Cancer. 2019. PMID: 31417642 Free PMC article.
-
Wolf-Hirschhorn Syndrome-Associated Genes Are Enriched in Motile Neural Crest Cells and Affect Craniofacial Development in Xenopus laevis.Front Physiol. 2019 Apr 12;10:431. doi: 10.3389/fphys.2019.00431. eCollection 2019. Front Physiol. 2019. PMID: 31031646 Free PMC article.
-
Retinoblastoma binding protein 2 (RBP2) promotes HIF-1α-VEGF-induced angiogenesis of non-small cell lung cancer via the Akt pathway.PLoS One. 2014 Aug 27;9(8):e106032. doi: 10.1371/journal.pone.0106032. eCollection 2014. PLoS One. 2014. PMID: 25162518 Free PMC article.
-
Genetic and epigenetic landscape of IDH-wildtype glioblastomas with FGFR3-TACC3 fusions.Acta Neuropathol Commun. 2020 Nov 9;8(1):186. doi: 10.1186/s40478-020-01058-6. Acta Neuropathol Commun. 2020. PMID: 33168106 Free PMC article.
-
High expression of TACC3 in esophageal squamous cell carcinoma correlates with poor prognosis.Oncotarget. 2015 Mar 30;6(9):6850-61. doi: 10.18632/oncotarget.3190. Oncotarget. 2015. PMID: 25760075 Free PMC article.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous
