Biochemical and Biophysical Research Communications, Vol.501, No.4, 913-919, 2018
TGF-beta 1 induced fascinl expression facilitates the migration and invasion of kidney carcinoma cells through ERK and JNK signaling pathways
Transforming growth factor-beta 1 (TGF-beta 1) plays a crucial role in the signaling network that controls cellular invasion and motility capability during tumor development. To investigate whether fascin1 plays a crucial role in TGF-beta 1-facilitated invasion and migration of kidney cancer cells (KCC), real-time PCR and western blotting were used to test the fascin1 expression after TGF-beta 1 treatment (10 ng/ml) in 769-P and OSRC cells. Fascin1 was silenced using the small interfering RNA (siRNA) technique. Cytoskeleton staining was used to test the change of Cytoskeleton. Cell migration and invasion changes were measured by wound-healing and Transwell assay. The results indicate that mRNA and protein levels of fascinl were dramatically increased after treatment with 10 ng/ml TGF-beta 1 in 769-P and OSRC cells. TGF-beta 1 promoted the occurrence of EMT (Epithelial-Mesenchymal Transition) and the invasive and migratory capabilities of the two cell lines after treatment with 10 ng/ml TGF-beta 1. In addition, fascinl siRNA dramatically attenuated the invasiveness and migration induced by TGF-beta 1. Furthermore, we identified that specific inhibitors of ERK and INK signaling pathways, FR180204 and SP600125, can suppress TGF-beta 1-induced fascinl expression. In conclusion, these results reveal that fascinl is an important mediator of TGF-beta 1-induced invasion and migration of KCC through ERK and JNK signal pathways. (C) 2018 Elsevier Inc. All rights reserved.