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Cofilin 1 induces the epithelial-mesenchymal transition of gastric cancer cells by promoting cytoskeletal rearrangement.

Abstract
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.
AuthorsHaibo Wang, Lide Tao, Feng Jin, Hao Gu, Xiaojun Dai, Tengyang Ni, Jun Feng, Yanbing Ding, Weiming Xiao, Yayun Qian, Yanqing Liu
JournalOncotarget (Oncotarget) Vol. 8 Issue 24 Pg. 39131-39142 (Jun 13 2017) ISSN: 1949-2553 [Electronic] United States
PMID28388575 (Publication Type: Journal Article)
Chemical References
  • Biomarkers, Tumor
  • CFL1 protein, human
  • Cofilin 1
  • Transforming Growth Factor beta1
Topics
  • Adult
  • Aged
  • Aged, 80 and over
  • Animals
  • Apoptosis
  • Biomarkers, Tumor (metabolism)
  • Case-Control Studies
  • Cell Proliferation
  • Cofilin 1 (metabolism)
  • Cytoskeleton (metabolism, pathology)
  • Epithelial-Mesenchymal Transition
  • Female
  • Gastric Mucosa (metabolism)
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Middle Aged
  • Prognosis
  • Signal Transduction
  • Stomach (pathology)
  • Stomach Neoplasms (metabolism, pathology)
  • Transforming Growth Factor beta1
  • Tumor Cells, Cultured
  • Xenograft Model Antitumor Assays

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