Cofilin 1 induces the epithelial-mesenchymal transition of gastric cancer cells by promoting cytoskeletal rearrangement
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Haibo Wang1,2,3,4,*, Lide Tao1,3,*, Feng Jin1,2,3,4,*, Hao Gu3,4, Xiaojun Dai3,4, Tengyang Ni1,2,3,4, Jun Feng1,2,3,4, Yanbing Ding1, Weiming Xiao1, Yayun Qian3,4 and Yanqing Liu1,2,3,4
1The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou 225000, China
2Clinical Medicine College of Yangzhou University, Yangzhou 225000, China
3The State Administration of Traditional Chinese Medicine Key Laboratory of Toxic Pathogens-Based Therapeutic Approaches to Gastric Cancer, Yangzhou 225000, China
4Institution of Combining Chinese Traditional and Western Medicine, Medical College, Yangzhou University, Yangzhou 225000, China
*These authors have contributed equally to this work and should be considered as co-first authors
Yanqing Liu, email: email@example.com
Yayun Qian, email: firstname.lastname@example.org
Keywords: CFL1, gastric cancer (GC), cytoskeleton rearrangement, epithelial-mesenchymal transition (EMT)
Received: January 12, 2017 Accepted: March 02, 2017 Published: March 27, 2017
Epithelial-mesenchymal transition (EMT) is an important biological process whereby malignant tumor cells obtain the ability to migrate, invade, resist apoptosis and degrade the extracellular matrix. We found that Cofilin1 (CFL1) expression was elevated in clinical gastric cancer specimens and correlated with biomarkers of EMT in BGC-823 gastric cancer cells. BGC-823 cells exhibited EMT phenotypes and increased metastatic ability when induced by TGF-β1. By contrast, BGC-823 cells transfected with Lv-siRNA-CFL1 did not exhibit EMT phenotypes under the same inducing conditions. As CFL1 expression increased, EMT cell filopodia stretched out. In addition, the ultrastructures observed using transmission electron microscopy indicated that silencing of CFL1 markedly inhibited depolymerization of fibrous actin and cytoskeletal reorganization during EMT. Similar results were obtained in vivo. These findings demonstrate that CFL1 induces EMT by promoting cytoskeletal rearrangement. Our results may provide the basis for developing new anticancer drugs to inhibit CFL1.
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