Abstract
TAZ, a WW-domain-containing transcriptional co-activator, is important for development of various tissues in mammals. Recently, TAZ has been found to be overexpressed in some types of human cancers. However, the role of TAZ in glioblastoma remains unclear. In this study, we found that TAZ was overexpressed in prognostically poor glioblastoma patients. Through knocking down or overexpressing TAZ in U87 and LN229 cells, the expression level of TAZ was found to be positively related to cell proliferation in vitro and tumor formation in vivo. Further investigation indicated that TAZ could significantly promote the acceleration of cell cycle. Moreover, the western blot for p-EGFR, p-AKT, p-ERK1/2, p21, cyclin E and CDK2 proteins, target genes of the EGFR pathway, indicated that TAZ significantly activated EGFR/AKT/ERK signaling. Additionally, the blockage of EGFR pathway resulted in a significantly inhibition of cell proliferation induced by TAZ. Taken together, these results demonstrate that TAZ can promote proliferation and tumor formation in glioblastoma cells by potentiating the EGFR/AKT/ERK pathway, and provide the evidence for promising target for the treatment of glioblastoma.
Highlights
Glioblastoma (GBM) is a common and primary brain tumor, with poor prognosis and few therapeutic advances in the last decade
These results demonstrate that TAZ can promote proliferation and tumor formation in glioblastoma cells by potentiating the epidermal growth factor receptor (EGFR)/AKT/ERK pathway, and provide the evidence for promising target for the treatment of glioblastoma
Most recently, enhanced expression of TAZ has been found in many malignant tumors, including gastric cancer, oral cancer, non-small cell lung cancer (NSCLC), breast cancer and neuroblastoma [11,12,13,14]
Summary
Glioblastoma (GBM) is a common and primary brain tumor, with poor prognosis and few therapeutic advances in the last decade. The genetic, bacterial virulence, environmental, and other factors have been in regulating the GBM process, but the molecular mechanism is weakly understood [4]. TAZ could bind with many transcription factors such as the RUNX family, Pax, TBX5, TIF-1 and READ [7,8,9]. TAZ was identified as a component of HippoLATS pathway, which is participated in transcriptional outcome to promote cell proliferation and inhibit apoptosis [10]. Most recently, enhanced expression of TAZ has been found in many malignant tumors, including gastric cancer, oral cancer, non-small cell lung cancer (NSCLC), breast cancer and neuroblastoma [11,12,13,14]. The role of TAZ in regulating tumor progression in glioblastoma cells has not been explored
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
