Lentivirus‑mediated knockdown of chondroitin polymerizing factor inhibits glioma cell growth in vitro

Oncol Rep. 2017 Aug;38(2):1149-1155. doi: 10.3892/or.2017.5731. Epub 2017 Jun 19.

Abstract

Glioma is the most common primary tumor in the central nervous system, characterized by rapid progression, aggressive behavior, frequent recurrence and poor prognosis. In the present study we demonstrated that chondroitin polymerizing factor (CHPF) is highly expressed in human glioma tissues and 4 glioma cell lines. To explore the role of CHPF in glioma, a lentiviral vector expressing CHPF shRNA was constructed and transfected into the glioma U251 cells, which stably downregulated the expression levels of the CHPF gene in U251 cells in vitro. U251 cell proliferation inhibition rates were determined by MTT assay. The effect of survivin shRNA on U251 cell cycle distribution and cell apoptosis was determined by flow cytometry. Compared to the shRNA‑Ctrl group of cells, the shRNA-CHPF group of cells exhibited decreased proliferation and a significant increase in the proportion of cells in the G0/G1 phase. In addition, we found that knockdown of the expression of CHPF increased apoptosis in glioma U251 cells. Therefore, our results confirmed that CHPF promotes growth and inhibits apoptosis in glioma U251 cells. Thus, by in vivo and in vitro data, the present study suggests that CHPF could be a new potential therapeutic target for glioma.

MeSH terms

  • Apoptosis
  • Biomarkers, Tumor
  • Brain Neoplasms / genetics
  • Brain Neoplasms / pathology
  • Brain Neoplasms / prevention & control*
  • Cell Cycle
  • Follow-Up Studies
  • Glioma / genetics
  • Glioma / pathology
  • Glioma / prevention & control*
  • Humans
  • In Vitro Techniques
  • Lentivirus / genetics*
  • N-Acetylgalactosaminyltransferases / antagonists & inhibitors*
  • N-Acetylgalactosaminyltransferases / genetics
  • Prognosis
  • RNA Interference
  • RNA, Small Interfering / genetics*
  • Tumor Cells, Cultured

Substances

  • Biomarkers, Tumor
  • RNA, Small Interfering
  • N-Acetylgalactosaminyltransferases
  • chondroitin synthase