Involvement of nuclear protein C23 in activation of EGFR signaling in cervical cancer

Tumour Biol. 2016 Jan;37(1):905-10. doi: 10.1007/s13277-015-3889-x. Epub 2015 Aug 10.

Abstract

Nuclear protein C23 and epidermal growth factor receptor (EGFR) are reported to be correlated with cervical cancer (CC). However the correlations between C23 and EGFR were rarely reported. Here, this study explored the effects of C23 in activation of EGFR signaling pathway. In our study, immunohistochemistry was used to identify the expression of C23 or EGFR in CC tissues. The level of the phosphorylated EGFR was observed by western blot, and cell invasion capacity was detected by Transwell assay. In this study, we found that C23 and EGFR were highly expressed in cervical cancer tissues, while C23 on the cell surface mainly expressed in CC tissues with lymph node metastasis, and was correlated to EGFR statistically. In vitro, western blot showed that either anti-C23 or anti-EGFR antibodies can inhibit the phosphorlation of EGFR with significant differences (p < 0.01). Besides, based on Transwell assay, the number of membrane-invading cells was reduced significantly in anti-C23 group, and no significant difference was found compared with anti-EGFR treatment (p > 0.05). In conclusion, C23 on the cell surface may be a kind of indispensable component in activation of EGFR signaling, by which C23 can participate in the growth and invasion of tumors. C23 antagonists may provide a new field for cervical cancer therapy.

Keywords: Activation; C23; CC; Epidermal growth factor receptor.

MeSH terms

  • Adult
  • Cell Line, Tumor
  • Cell Membrane / metabolism
  • Cell Movement
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Lymphatic Metastasis
  • Middle Aged
  • Nuclear Proteins / metabolism
  • Nucleolin
  • Phosphoproteins / metabolism*
  • RNA-Binding Proteins / metabolism*
  • Signal Transduction
  • Uterine Cervical Neoplasms / genetics
  • Uterine Cervical Neoplasms / metabolism*

Substances

  • Nuclear Proteins
  • Phosphoproteins
  • RNA-Binding Proteins
  • EGFR protein, human
  • ErbB Receptors