题名 | Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway |
作者 | |
通讯作者 | Zuo,You |
发表日期 | 2021-08-01
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DOI | |
发表期刊 | |
ISSN | 0895-8696
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EISSN | 1559-1166
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卷号 | 71期号:8页码:1636-1647 |
摘要 | The present study aimed to detect the effect of tenascin C (TNC) on cell function and chemosensitivity to paclitaxel and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling in glioma cells. Human glioma cells U87, LN-229, T98G and U251 and normal human astrocytes were obtained, in which TNC expression was detected. The U87 cells and U251 cells were chosen and infected with lentivirus of control overexpression, TNC overexpression, control knockdown, and TNC knockdown for functional experiments. Rescue experiments were then performed to evaluate the effect of PI3K/AKT activator 740 Y-P on cell function and chemosensitivity to paclitaxel in TNC knockdown U251 cells. TNC mRNA and protein expression was elevated in glioma cells, including U87, LN-229, U251 and T98G cells, compared to normal human astrocytes. In U87 and U251 cells, TNC promoted proliferation while inhibiting apoptosis. In addition, TNC upregulated PI3K and p-AKT protein expression in U87 and U251 cells. As for chemosensitivity, TNC increased relative viability in U251 cells treated with 400 ng/mL and 800 ng/mL paclitaxel. In terms of stemness, TNC increased the sphere number per 1000 cells, CD44CD133 cell percentage and 1/stem cell frequency (assessed by extreme limiting dilution analysis) in U251 cells. In rescue experiments, 740 Y-P reduced the effect of TNC on proliferation, apoptosis, chemosensitivity to paclitaxel, and stemness in U251 cells. TNC acts as an oncogenic factor by promoting cancer cell proliferation and stemness while inhibiting apoptosis and chemosensitivity to paclitaxel in glioma via modulation of PI3K/AKT signaling. |
关键词 | |
相关链接 | [Scopus记录] |
收录类别 | |
语种 | 英语
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学校署名 | 通讯
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WOS记录号 | WOS:000641243900001
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ESI学科分类 | NEUROSCIENCE & BEHAVIOR
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Scopus记录号 | 2-s2.0-85111969922
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来源库 | Scopus
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引用统计 |
被引频次[WOS]:13
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成果类型 | 期刊论文 |
条目标识符 | http://sustech.caswiz.com/handle/2SGJ60CL/242725 |
专题 | 南方科技大学盐田医院 南方科技大学第二附属医院 |
作者单位 | 1.Department of Neurosurgery,Huazhong University of Science and Technology Union Shenzhen Hospital,The 6th Affiliated Hospital of Shenzhen University Health Science Center (Shenzhen Nanshan People’s Hospital),Guangdong,Shenzhen 518056,China 2.Department of Neurosurgery,The Seventh Affiliated Hospital of Sun Yat-Sen University,Shenzhen,China 3.Department of Biostatistics and Epidemiology,School of Public Health,Shenzhen University Health Science Center,Guangdong,Shenzhen 518060,China 4.Department of Neurosurgery,Southern University of Science and Technology Yantian Hospital,Guangdong,Shenzhen 518081,China |
通讯作者单位 | 南方科技大学盐田医院 |
推荐引用方式 GB/T 7714 |
Zhang,Qingping,Xu,Binchu,Hu,Fulan,et al. Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway[J]. JOURNAL OF MOLECULAR NEUROSCIENCE,2021,71(8):1636-1647.
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APA |
Zhang,Qingping.,Xu,Binchu.,Hu,Fulan.,Chen,Xianjin.,Liu,Xinmin.,...&Zuo,You.(2021).Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway.JOURNAL OF MOLECULAR NEUROSCIENCE,71(8),1636-1647.
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MLA |
Zhang,Qingping,et al."Tenascin C Promotes Glioma Cell Malignant Behavior and Inhibits Chemosensitivity to Paclitaxel via Activation of the PI3K/AKT Signaling Pathway".JOURNAL OF MOLECULAR NEUROSCIENCE 71.8(2021):1636-1647.
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