Effects of tachyplesin I on human U251 glioma stem cells

Ding,Hong; Jin,Gang; Zhang,Lijun; Dai,Jianguo; Dang,Jianzhang; Han,Yali

doi:10.3892/mmr.2014.3021

Effects of tachyplesin I on human U251 glioma stem cells

Authors:
- Hong Ding
- Gang Jin
- Lijun Zhang
- Jianguo Dai
- Jianzhang Dang
- Yali Han
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Affiliations: Faculty of Chemical Engineering and Light Industry, Guangdong University of Technology, Guangzhou, Guangdong 510006, P.R. China, School of Applied Chemistry and Biotechnology, Shenzhen Polytechnic, Shenzhen Public Technology Service Platform for Scale Cell Culture Techniques and Cell Resource, Shenzhen, Guangdong 518055, P.R. China
Published online on: November 28, 2014 https://doi.org/10.3892/mmr.2014.3021
Pages: 2953-2958

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Abstract

Glioblastoma, is one of the most malignant types of intracranial tumor with complex progressive cellular and underlying molecular events. The use of glioma stem cells (GSCs) offers a promising strategy for tumor therapy in the future. Tachyplesin I has been demonstrated to have potential anticancer activity and was first observed in leukocytes. In the present study, the GSC subset was isolated from U251 glioma cells and tachyplesin I was assessed for antitumor activity. As a result, the U251 cells exhibited certain GSC phenotypes, including the expression of stem cell biomarkers CD133 and nestin, when transferred into stem cell culture conditions. The GSCs were grown in an adherent manner in a medium containing serum, while the U251 glioma cells were suspended and cultured in serum‑free medium. Tachyplesin I damaged the structure of GSC and inhibited the culture of GSC spheres in a time and dose‑dependent manner. When tachyplesin I was administered at a concentration of 10‑40 µg/ml, GSC differentiation was induced. GSCs treated with a low dose of tachyplesin I disrupted the plasma membrane and led to a loss of cytoplasmic organelles. These findings indicated that tachyplesin I had an effect on inhibiting tumor stem cells and demonstrated that tachyplesin I inhibited GSCs by disrupting the plasma membranes and inducing GSC differentiation.

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