Oncogenic miR-106b-5p promotes cisplatin resistance in triple-negative breast cancer by targeting GDF11

被引:0
|
作者
Zhou, Qing [1 ,2 ,3 ,4 ]
Hu, Qinglin [1 ,2 ]
机构
[1] Chengdu Med Coll, Clin Med Coll, Thyroid & Breast Surg, Chengdu, Sichuan, Peoples R China
[2] Chengdu Med Coll, Affiliated Hosp 1, Chengdu, Sichuan, Peoples R China
[3] Chengdu Med Coll, Clin Med Coll, Thyroid & Breast Surg, 278,Middle Sect Baoguang Ave, Chengdu 610500, Sichuan, Peoples R China
[4] Chengdu Med Coll, Affiliated Hosp 1, 278,Middle Sect Baoguang Ave, Chengdu 610500, Sichuan, Peoples R China
关键词
TNBC (triple-negative breast cancer); Cisplatin; miR-106b-5p; GDF11; MICRORNA; APOPTOSIS;
D O I
10.14670/HH-18-668
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
. Background. Cytoplatin (CDDP) is a standard treatment for triple -negative breast cancer (TNB), but patient resistance to CDDP limits its efficacy. A growing study confirms that microRNAs (miRNAs) are significantly important in breast cancer, especially TNBC. This research was carried out to examine the function of miR-106b-5p in CDDP resistance of TNBC as well as the downstream mechanism. Methods. The miR-106b-5p and growthdifferentiation factor 11 (GDF 11) expressions in the tissues from TNBC patients and CDDP-treated TNBC cell lines were measured by RT-qPCR. Thereafter, cell proliferation and migration in the presence of CDDP treatment were evaluated via CCK-8 and Transwell assays in the TNBC cells. A xenograft mice model was also established to verify the miR-106b-5p silencing effect on the growth of CDDP resistance TNBC cells in vivo. Luciferase reporter experiments were performed to predict the relationship between miR-106b-5p and GDF11 expression. Results. The results showed that miR-106b-5p was upregulated in the TNBC tumor cells and TNBC cells treated with CDDP and knockdown of this caused inhibition of the TNBC cell lines' proliferation, migration and suppressed the growth of the TNBC xenografted tumors, in the presence of CDDP treatment. In addition, it was observed that miR-106b-5p can bind to GDF11; as a result in the TNBC tissues and CDDPtreated TNBC cell lines the down -regulation of GDF11 was observed. Moreover, GDF11 silencing promoted CDDP-treated TNBC cell lines' proliferation and migration and reversed the interference effect of miR106b-5p. Conclusions. MiR-106b-5p was upregulated in TNBC and this upregulation may promote CDDP resistance of the TNBC cells by targeting GDF11 and inhibiting its expression.
引用
收藏
页码:533 / 541
页数:9
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