Effect of Tamibarotene on the proliferation and Tyrosine kinase receptor A,N-myc expressions of neuroblastoma SH-SY5Y cells
10.3760/cma.j.issn.2095-428X.2019.07.017
- VernacularTitle:他米巴罗汀对神经母细胞瘤SH-SY5Y细胞增殖及酪氨酸激酶受体A、N-myc表达的影响
- Author:
Jianying LIU
1
;
Aimin LI
;
Jianyong WANG
;
Xiaoli WANG
;
Li WANG
;
Yingying SI
Author Information
1. 青岛大学医学院附属烟台毓璜顶医院儿科 264000
- Keywords:
Tamibarotene;
Neuroblastoma SH-SY5Y cells;
Proliferation;
Tyrosine kinase receptor A;
N-myc gene
- From:
Chinese Journal of Applied Clinical Pediatrics
2019;34(7):546-548
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of Tamibarotene on the SH-SY5Y cell proliferation inhibition ability and the mRNA and protein expressions of tyrosine kinase receptor a (TrkA) and N-myc (MYCN) in order to provide some experimental bases for the treatment of neuroblastoma.Methods The SH-SY5Y cells were treated with different concentrations of Am80 (0,10,20,40,80,160 μmol/L) for 48 h,then Cell Counting Kit-8 (CCK-8) was used to test the cell proliferation.Reverse transcription PCR(RT-PCR) and Western blot were used to test the mRNA and protein expressions of TrkA and MYCN at 48 hours.Results When the concentration was 10 μmol/L,Am80 had no significant inhibitory effect on SH-SY5Y cells [(3.51 ± 1.68)％,inhibition ratio ＜ 5 ％];but when the concentration was 20 μmol/L,it showed weak inhibition [(9.60 ± 1.97) ％,inhibition ratio ＜ 10％].The inhibition rate of SH-SY5Y cell proliferation[(57.43 ± 4.95)％] was significantly enhanced at Am80 with a concentration of 80 μmol/L.The concentrations of Am80 could effectively inhibit SH-SY5Y cell proliferation in a dose-dependent manner(P ＜0.05).The expression of TrkA increased with the increase of Am80 concentration.Am80 significantly decreased the expression of MYCN in SH-SY5Y cells(10 μmol/L:0.65 ±0.05 vs.20 μmol/L:0.36 ±0.06),and the difference was statistically significant(P ＜ 0.05).Conclusions It is suggested that Am80 can effectively inhibit SH-SY5Y cell proliferation in a concentration-dependent manner.The underlying mechanism involves increasing the expression of TrkA by down-regulation of MYCN.
