Induction of neural differentiation in rat C6 glioma cells with taxol

Brain Behav. 2015 Oct 26;5(12):e00414. doi: 10.1002/brb3.414. eCollection 2015 Dec.

Abstract

Background: Glioblastoma is a common and aggressive type of primary brain tumor. Several anticancer drugs affect GBM (glioblastoma multiforme) cells on cell growth and morphology. Taxol is one of the widely used antineoplastic drugs against many types of solid tumors, such as breast, ovarian, and prostate cancers. However, the effect of taxol on GBM cells remains unclear and requires further investigation.

Methods: Survival rate of C6 glioma cells under different taxol concentrations was quantified. To clarify the differentiation patterns of rat C6 glioma cells under taxol challenge, survived glioma cells were characterized by immunocytochemical, molecular biological, and cell biological approaches.

Results: After taxol treatment, not only cell death but also morphological changes, including cell elongation, cellular processes thinning, irregular shapes, and fragmented nucleation or micronuclei, occurred in the survived C6 cells. Neural differentiation markers NFL (for neurons), β III-tubulin (for neurons), GFAP (for astrocytes), and CNPase (for oligodendrocytes) were detected in the taxol-treated C6 cells. Quantitative analysis suggested a significant increase in the percentage of neural differentiated cells. The results exhibited that taxol may trigger neural differentiation in C6 glioma cells. Increased expression of neural differentiation markers in C6 cells after taxol treatment suggest that some anticancer drugs could be applied to elimination of the malignant cancer cells as well as changing proliferation and differentiation status of tumor cells.

Keywords: Glioma; neural differentiation; taxol.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 2',3'-Cyclic-Nucleotide Phosphodiesterases / metabolism
  • Animals
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Blotting, Western
  • Brain Neoplasms / drug therapy*
  • Brain Neoplasms / pathology
  • Brain Neoplasms / physiopathology
  • Cell Death / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Dose-Response Relationship, Drug
  • Fluorescent Antibody Technique
  • Glial Fibrillary Acidic Protein / metabolism
  • Glioma / drug therapy*
  • Glioma / pathology
  • Glioma / physiopathology
  • Nestin / metabolism
  • Neurogenesis / drug effects*
  • Neurogenesis / physiology
  • Neurons / drug effects*
  • Neurons / pathology
  • Neurons / physiology
  • Paclitaxel / pharmacology*
  • RNA, Messenger / metabolism
  • Rats
  • Real-Time Polymerase Chain Reaction
  • Tubulin / metabolism

Substances

  • Antineoplastic Agents, Phytogenic
  • Glial Fibrillary Acidic Protein
  • Nes protein, rat
  • Nestin
  • RNA, Messenger
  • Tubb3 protein, rat
  • Tubulin
  • 2',3'-Cyclic-Nucleotide Phosphodiesterases
  • Paclitaxel