Curcumin attenuates lncRNA H19-induced epithelial-mesenchymal transition in tamoxifen-resistant breast cancer cells

被引:58
作者
Cai, Jiaqin [1 ]
Sun, Hong [1 ]
Zheng, Bin [2 ]
Xie, Mumu [1 ]
Xu, Chenxia [2 ]
Zhang, Guifeng [1 ]
Huang, Xuhui [1 ]
Zhuang, Jie [1 ]
机构
[1] Fujian Med Univ, Fujian Prov Hosp, Shengli Clin Med Coll, Dept Pharm, 134 Dong St, Fuzhou 350001, Fujian, Peoples R China
[2] Fujian Med Univ, Dept Pharm, Union Hosp, Fuzhou 350001, Fujian, Peoples R China
关键词
tamoxifen-resistance; epithelial-mesenchymal transition; breast cancer; H19 imprinted maternally expressed transcript; curcumin; EXPRESSION; THERAPY; SNAIL;
D O I
10.3892/mmr.2020.11651
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
The H19 long non-coding RNA is involved in the development of tamoxifen resistance in breast cancer. However, the relationship between H19 and the metastatic potential and treatment options for tamoxifen-resistant (TAMR) breast cancer is not completely understood. Curcumin inhibits cellular proliferation, migration and invasiveness in several cancer types, including pancreatic cancer, breast cancer and chronic myeloid leukemia. The present study aimed to investigate the role of H19 in MCF-7/TAMR cell epithelial-mesenchymal transition (EMT), migration and invasiveness, and to assess the ability of curcumin to inhibit H19-mediated effects. Reverse transcription-quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit-8, wound healing and Transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. H19 overexpression enhanced MCF-7/TAMR cell EMT, invasion and migration by upregulating Snail. Furthermore, curcumin notably decreased the expression levels of epithelial marker E-cadherin and markedly increased the expression levels of mesenchymal marker N-cadherin in MCF-7/TAMR cells compared with the control group. In addition, following treatment with curcumin for 48 h, H19 expression was decreased in a dose-dependent manner. Moreover, curcumin treatment for 48 h significantly attenuated H19-induced alterations in N-cadherin and E-cadherin expression levels. Curcumin also prevented H19-induced invasion and migration. The present study indicated that H19 may serve as a promoting factor of EMT, invasion and migration in MCF-7/TAMR cells, suggesting that curcumin may prevent H19-associated metastasis. Therefore, curcumin may serve as a promising therapeutic drug for patients with TAMR breast cancer.
引用
收藏
页数:9
相关论文
共 32 条
[11]
Histone deacetylase inhibitor induction of epithelial-mesenchymal transitions via up-regulation of Snail facilitates cancer progression [J].
Jiang, Guan-Min ;
Wang, Hong-Sheng ;
Zhang, Fan ;
Zhang, Kun-Shui ;
Liu, Zong-Cai ;
Fang, Rui ;
Wang, Hao ;
Cai, Shao-Hui ;
Du, Jun .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2013, 1833 (03) :663-671
[12]
Vimentin and epithelial-mesenchymal transition in human breast cancer - Observations in vitro and in vivo [J].
Kokkinos, Maria I. ;
Wafai, Razan ;
Wong, Meng Kang ;
Newgreen, Donald F. ;
Thompson, Erik W. ;
Waltham, Mark .
CELLS TISSUES ORGANS, 2007, 185 (1-3) :191-203
[13]
Curcumin enhances the radiosensitivity of renal cancer cells by suppressing NF-κB signaling pathway [J].
Li, Gang ;
Wang, Ziming ;
Chong, Tie ;
Yang, Jie ;
Li, Hongliang ;
Chen, Haiwen .
BIOMEDICINE & PHARMACOTHERAPY, 2017, 94 :974-981
[14]
Curcumin inhibits superoxide dismutase-induced epithelial-to-mesenchymal transition via the PI3K/Akt/NF-B pathway in pancreatic cancer cells [J].
Li, Wei ;
Jiang, Zhengdong ;
Xiao, Xue ;
Wang, Zheng ;
Wu, Zheng ;
Ma, Qingyong ;
Cao, Lei .
INTERNATIONAL JOURNAL OF ONCOLOGY, 2018, 52 (05) :1593-1602
[15]
Long non-coding RNA H19 promotes the proliferation and invasion of lung cancer cells and regulates the expression of E-cadherin, N-cadherin, and vimentin [J].
Liaol, Shu ;
Yu, Chaxiu ;
Liu, Hucheng ;
Zhang, Congkai ;
Li, Yong ;
Zhongl, Xiaojun .
ONCOTARGETS AND THERAPY, 2019, 12 :4099-4106
[16]
Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔCT method [J].
Livak, KJ ;
Schmittgen, TD .
METHODS, 2001, 25 (04) :402-408
[17]
Mechanisms of resistance in estrogen receptor positive breast cancer: overcoming resistance to tamoxifen/aromatase inhibitors [J].
Mills, Jamie N. ;
Rutkovsky, Alex C. ;
Giordano, Antonio .
CURRENT OPINION IN PHARMACOLOGY, 2018, 41 :59-65
[18]
Involvement of the P2X7 receptor in the migration and metastasis of tamoxifen-resistant breast cancer: effects on small extracellular vesicles production [J].
Park, Miso ;
Kim, Jieun ;
Nguyen T T Phuong ;
Park, Jung Gyu ;
Park, Jin-Hee ;
Kim, Yong-Chul ;
Baek, Moon Chang ;
Lim, Sung Chul ;
Kang, Keon Wook .
SCIENTIFIC REPORTS, 2019, 9 (1)
[19]
H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance [J].
Peng, Fei ;
Li, Ting-Ting ;
Wang, Kai-Li ;
Xiao, Guo-Qing ;
Wang, Ju-Hong ;
Zhao, Hai-Dong ;
Kang, Zhi-Jie ;
Fan, Wen-Jun ;
Zhu, Li-Li ;
Li, Mei ;
Cui, Bai ;
Zheng, Fei-Meng ;
Wang, Hong-Jiang ;
Lam, Eric W-F ;
Wang, Bo ;
Xu, Jie ;
Liu, Quentin .
CELL DEATH & DISEASE, 2017, 8 :e2569-e2569
[20]
LncRNA-mediated regulation of cell signaling in cancer [J].
Peng, W-X ;
Koirala, P. ;
Mo, Y-Y .
ONCOGENE, 2017, 36 (41) :5661-5667