کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8838843 | 1613217 | 2018 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
RNAi-mediated SYT14 knockdown inhibits the growth of human glioma cell line U87MG
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موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: RNAi-mediated SYT14 knockdown inhibits the growth of human glioma cell line U87MG RNAi-mediated SYT14 knockdown inhibits the growth of human glioma cell line U87MG](/preview/png/8838843.png)
چکیده انگلیسی
SYT14 (Synaptotagmin 14) participates in pathomechanical neurodegeneration and contributes to abnormal neurodevelopment. However, the functional mechanism of SYT14 in human glioma tumorigenesis remains unclear. In the present study, we measured the expression levels of SYT14 mRNA in human glioma cell lines, U373MG, U178, and U87MG and neural stem cells (NSC) cell line by RT-PCR, and used lentivirus-mediated small hairpin RNAs (shRNAs) to knock down SYT14 expression in U87MG cells. Changes in SYT14 expression were determined by real-time PCR. Cell proliferation and colony formation assays were used to analyze the role of SYT14 in U87MG cell proliferation, and cell apoptosis was assessed by flow cytometry. SYT14 mRNA expression was detected in the three glioma cell lines, and was highest in the U87MG cell line. The RNAi-mediated knockdown of SYT14 significantly decreased cell proliferation and colony formation in U87MG cells, and caused a moderate increase in apoptosis. Fewer S phase cells and more G2/M phase cells were observed. These data indicate that SYT14 is highly expressed in glioma cells, and may participate in glioma cell proliferation, apoptosis, and colony formation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research Bulletin - Volume 140, June 2018, Pages 60-64
Journal: Brain Research Bulletin - Volume 140, June 2018, Pages 60-64
نویسندگان
Bin Sheng, Yuxin Jiang, Degang Wu, Niansheng Lai, Zhennan Ye, Bingbing Zhang, Xinggen Fang, Shanshui Xu,