17β-Estradiol treatment inhibits breast cell proliferation, migration and invasion by decreasing MALAT-1 RNA level

被引:175
作者
Zhao, Ziyi [1 ]
Chen, Changjin [2 ]
Liu, Yu [1 ]
Wu, Chuanfang [1 ]
机构
[1] Sichuan Univ, Key Lab Bioresources & Ecoenvironm, Coll Life Sci, Minist Educ, Chengdu 610041, Peoples R China
[2] Sichuan Univ, Dept Pediat, West China Univ Hosp 2, Chengdu 610041, Peoples R China
关键词
17; beta-Estradiol; MALAT-1; Proliferation; Migration; Invasion; Breast cells; NONCODING RNA; SHORT-TERM; ESTROGEN; CANCER; METABOLITES; MECHANISMS;
D O I
10.1016/j.bbrc.2014.02.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Breast cancer cells, which express estrogen receptor alpha (ER alpha), respond to estrogen in a concentration dependent fashion, resulting in proliferation or apoptosis. But breast cancer cells without ER alpha show no effect on low concentration of estrogen treatment. Proliferation, migration and invasion of MCF10a, MCF7 and MB231 cells treated with low (1 nM) or high (100 nM) dose of 17 beta-Estradiol (E2) was performed. We identified the effects of E2 on these breast cell lines, and looked for the difference in the presence and absence of ER alpha. Specifically, we looked for the changes of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1), which is found extensively and highly expressed in several kinds of tumor cells, including breast carcinoma. It was observed that proliferation, migration and invasion of breast cells were greatly affected by high concentration E2 treatment and were not affected by low concentration E2 treatment in an ERa independent way. We found that the high concentration E2 treatment largely decreased MALAT-1 RNA level. Interestingly, MALAT-1 decreasing by knocking down showed similar effects on proliferation, migration and invasion. E2 treatment affects breast tumor or non-tumor cells proliferation, migration and invasion in an ER alpha -independent, but a dose-dependent way by decreasing the MALAT-1 RNA level. (C) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:388 / 393
页数:6
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