Effect of interference of SNCG gene on radiosensitivity of breast cancer T47D cells / 中华放射医学与防护杂志
Chinese Journal of Radiological Medicine and Protection
; (12): 19-23, 2017.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-506994
Biblioteca responsável:
WPRO
ABSTRACT
Objective To explore the role of γ-synuclein(SNCG) siRNA in the radiosensitivity of breast cancer T47D cells.Methods SNCG siRNA was synthesized according to the coding sequence of SNCG mRNA and then transiently transferred into T 47D cell with lipofectamine .The expression of SNCG gene and protein was detected by RT-PCR and Western-blot, respectively.Cells were divided into three groups, SNCG siRNA interference group , negative control group and blank control group , which were irradiated with different doses of 60 Coγ-rays.Cell radiosensitivity was evaluated by colony formation assay , cell proliferation was assayed by CCK-8 kit, and the protein expressions of phosphorylated-AKT and mTOR were detected by Western blot assay .Results Compared with blank control cells , the expressions of SNCG gene and protein in the SNCG siRNA transferred T 47D cells were efficiently diminished .Cell colony formation results showed that , under 4, 6, 8 Gy irradiation, the cell survival of siRNA transfection group was lower than that of control group (t=5.449, 8.882, 21.503, P<0.05).CCK-8 experiments showed that the cell proliferation abilities of siRNA group at 24, 48, 72 h after 6 Gy irradiation were lower than those of control group (t=5.603, 4.839, 6.115, P<0.05).In addition, after 6 Gy irraddaition, the AKT and mTOR phosphorylation levels in the siRNA group were more obviously reduced compared with blank groups , but the total AKT and mTOR had no changes .Conclusions Transfection of SNCG siRNA can enhance the radiosensitivity of breast cancer cells probably by inhibiting p -AKT signal pathway .
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Journal of Radiological Medicine and Protection
Ano de publicação:
2017
Tipo de documento:
Artigo