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  3. Anatomy and Cell Biology / 解剖學暨細胞生物學研究所
  4. Induction of neural differentiation in rat C6 glioma cells with taxol
 
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Induction of neural differentiation in rat C6 glioma cells with taxol

Journal
Brain and Behavior
Journal Volume
5
Journal Issue
12
Pages
1-10
Date Issued
2015
Author(s)
Chao C.-C.
Kan D.
Lo T.-H.
KUO-SHYAN LU  
CHUNG-LIANG CHIEN  
DOI
10.1002/brb3.414
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84954400088&doi=10.1002%2fbrb3.414&partnerID=40&md5=8545aba5201adf06b5d5f74911deff46
https://scholars.lib.ntu.edu.tw/handle/123456789/466421
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), βIII-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. ? 2015 Published by Wiley Periodicals, Inc.
SDGs

[SDGs]SDG3

Other Subjects
2',3' cyclic nucleotide 3' phosphodiesterase; beta III tubulin; beta tubulin; glial fibrillary acidic protein; messenger RNA; paclitaxel; unclassified drug; antineoplastic agent; glial fibrillary acidic protein; messenger RNA; Nes protein, rat; nestin; paclitaxel; Tubb3 protein, rat; tubulin; animal cell; Article; cell elongation; cell proliferation; cell survival; confocal microscopy; controlled study; glioblastoma; glioma cell; immunocytochemistry; immunofluorescence; MTT assay; nerve cell differentiation; nonhuman; priority journal; protein expression; rat; real time polymerase chain reaction; reverse transcription polymerase chain reaction; upregulation; Western blotting; animal; Brain Neoplasms; cell death; dose response; drug effects; fluorescent antibody technique; glioma; metabolism; nerve cell; nervous system development; pathology; pathophysiology; physiology; tumor cell line; 2',3'-Cyclic-Nucleotide Phosphodiesterases; Animals; Antineoplastic Agents, Phytogenic; Blotting, Western; Brain Neoplasms; Cell Death; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Fluorescent Antibody Technique; Glial Fibrillary Acidic Protein; Glioma; Nestin; Neurogenesis; Neurons; Paclitaxel; Rats; Real-Time Polymerase Chain Reaction; RNA, Messenger; Tubulin
Publisher
John Wiley and Sons Ltd
Type
journal article

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