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    Knockdown of CPEB4 expression suppresses cell migration and invasion via Akt pathway in non-small cell lung cancer.

    • Authors:
    • Jing Hu
      1 State Key Laboratory for Infectious Disease Prevention and Control
      China
      Libin Zhang
      University of Nebraska Medical Center
      United States
      Dr. Qiang Chen, PhD
      Arizona State University
      Professor
      United States
      Jie Lin
      The First Affiliated Hospital of Wenzhou Medical University
      United States
      Shaobo Wang
      Wuhan Institute of Virology
      China
      Ri Liu
      School of Chinese Materia Medica
      Wenjing Zhang
      MOE Key Laboratory of Macromolecular Synthesis and Functionalization
      China
      Kun Miao
      Roche Innovation Center Shanghai
      Tao Shou
      The First People's Hospital of Yunnan Province
      Kunming Shi | China
    Cell Biol Int 2017 Dec 29. Epub 2017 Dec 29.
    Department of Medical Oncology, First People's Hospital of Yunnan Province, No. 157 of Jinbi Road, Xishan district of Kunming City, Yunnan Province, P. R. China.
    Cytoplasmic polyadenylation element binding protein 4 (CPEB4) could be an important regulator in variety of cancers. However, the biological function and the underlying molecular mechanism of CPEB4 in non-small cell lung cancer (NSCLC) remains unknown. In this study, we investigated the metastasis role of CPEB4 in NSCLC cells, we knocked down CPEB4 using siRNA. Transwell migration assay and cell invasion assay on Matrigel were presented, and cell migration was also determined by scratch-healing assay. ROS generation were determined by fluorescence probe DCFH2-DA. The protein expression was assessed by ELISA and Western blot analysis. LY294002 were used to inhibit PI3 K/Akt signaling. The data showed that knockdown of CPEB4 inhibited the migration and invasion of NSCLC. Moreover, silencing of CPEB4 reduced Snail and MMP-3 expression in vitro. We also indicated that CPEB4 knockdown increased the ROS expression. Furthermore, we found that silencing of CPEB4 decreased pAkt expression. Taken all together, our data demonstrated that silencing of CPEB4 induces ROS generation, thus suppressing the Akt expression, which finally prevents NSCLC cells invasion and migration. Therefore, CPEB4 may regard as a target to inhibit NSCLC invasion and metastasis through Akt pathway.
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