Synaptotagmin-7, a binding protein of P53, inhibits the senescence and promotes the tumorigenicity of lung cancer cells

Biosci Rep. 2019 Feb 8;39(2):BSR20181298. doi: 10.1042/BSR20181298. Print 2019 Feb 28.

Abstract

Lung cancer has been one of the most common malignancies in the world. Cell senescence has been recognized as the avenue to inhibit tumor progression. However, the mechanisms remain poorly understood. In the present study, we have shown that synaptotagmin-7 (SYT7) expression was up-regulated in lung cancer. SYT7 also promoted the growth and colony formation of lung cancer cells and inhibited their senescence. In a molecular mechanism study, SYT7 was shown to interact with P53 and to potentiate the interaction between P53 and MDM2. Taken together, the present study demonstrates the oncogenic roles of SYT7 in lung cancer, and suggests that SYT7 may be a good therapeutic target for lung cancer treatment.

Keywords: Lung cancer; P53; SYT7; Senescence.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • A549 Cells
  • Cell Line, Tumor
  • Cellular Senescence
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / mortality
  • Lung Neoplasms / pathology*
  • Proto-Oncogene Proteins c-mdm2 / metabolism
  • Synaptotagmins / genetics
  • Synaptotagmins / metabolism*
  • Tumor Stem Cell Assay
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • CDKN1A protein, human
  • CDKN2A protein, human
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • SYT7 protein, human
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Synaptotagmins
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2