Suppressing stathmin-l can inhibit chkl protein expression and reduce the invasion and tumorigenicity of cervical cancer cells

Eur J Gynaecol Oncol. 2017;38(2):271-276.

Abstract

The purpose of this study was to evaluate the effects of stathmin-l on chkl protein expression in cervical cancer cells and the influ- ences on the cells' invasion and tumorigenicity. Suppressed stathmin-l expression in Hela cells and C33A cells by lentiviral vector were utilized. Real time PCR and Western blot were used to examine the expression of chkl. Cell proliferation and invasion were stud- ied using MTT assays and transwell migration assays.The differences of tumorigenicity in vivo were explored using xenograft experi- ments. In addition, stathmin-l expressions in 24 cervical cancer patients were studied without regional lymph nodes metastasis and 16 metastatic patients by immunohistochemistry assays and real time PCR. This study found downregulating stathmin-l reduced chkl ex- pressions and the proliferation and invasion in cervical cancer cells and reduced the tumorigenicity of tumor cells.

MeSH terms

  • Animals
  • Carcinogenesis / genetics
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Checkpoint Kinase 1 / metabolism*
  • Female
  • Genetic Vectors
  • HEK293 Cells
  • HeLa Cells
  • Humans
  • Lymphatic Metastasis
  • Mice
  • Mice, SCID
  • Neoplasm Invasiveness
  • Neoplasm Transplantation
  • RNA, Small Interfering
  • Stathmin / genetics*
  • Uterine Cervical Neoplasms / metabolism*
  • Uterine Cervical Neoplasms / pathology*

Substances

  • RNA, Small Interfering
  • STMN1 protein, human
  • Stathmin
  • CHEK1 protein, human
  • Checkpoint Kinase 1