Abstract:
BACKGROUND:Glioma is the most common human central nervous system tumour with a high degree of malignancy. Some Rab GTPases have significant effects on glioma. OBJECTIVE:This study aimed to investigate the effect of Rab3b (Rab GTPase3b) on human glioma cell proliferation and apoptosis by silencing Rab3b and to initially verify the value of Rab3b expression for the diagnosis and progression in human glioma. METHODS:Rab3b was silenced by siRNA transfection. Human glioma tissues and normal brain tissues adjacent to glioma were obtained by surgery. Rab3b, P53, Caspase 7, Bax, and Bim mRNA and protein expression levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell proliferation was detected by the cell counting kit-8 assay, and the cell cycle and apoptosis were analysed using flow cytometry. RESULTS:Rab3b mRNA and protein expression in human glioma U251 and U87 cells was significantly downregulated after Rab3b silencing. Rab3b silencing inhibited glioma cell proliferation by promoting cell cycle arrest and induced apoptosis by upregulating the expression of apoptosis-related proteins. Rab3b expression in human glioma (n = 33) was significantly higher than that in normal brain tissues adjacent to glioma (n = 15). In addition, Rab3b expression levels in high-grade gliomas (WHO III-IV, n = 19) were also significantly higher than those in low-grade gliomas (WHO I-II, n = 14). CONCLUSION:Rab3b expression levels are significantly related to the progression of gliomas. Moreover, Rab3b silencing not only significantly inhibits cell proliferation in gliomas via cell cycle arrest but also promotes cell apoptosis by upregulating the expression levels of apoptosis-related proteins, however these preliminary in vitro results warrant validation on in vivo studies.
journal_name
Curr Pharm Desjournal_title
Current pharmaceutical designauthors
Luo Q,Liu Y,Yuan Z,Huang L,Diao Bdoi
10.2174/1381612826666200917145228subject
Has Abstractpub_date
2020-09-17 00:00:00eissn
1381-6128issn
1873-4286pii
CPD-EPUB-110024pub_type
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