Downregulation of long noncoding RNA MALAT1 induces epithelial-to-mesenchymal transition via the PI3K-AKT pathway in breast cancer

被引：6
|
作者：
Xu, Shouping [1 ]
Sui, Shiyao [1 ]
Zhang, Jinfeng [1 ]
Bai, Nanxia [1 ]
Shi, Qingyu [1 ]
Zhang, Guangwen [2 ]
Gao, Song [1 ]
You, Zilong [1 ]
Zhan, Chao [1 ]
Liu, Feng [1 ]
Pang, Da [1 ,3 ,4 ,5 ]
机构：
[1] Harbin Med Univ, Canc Hosp, Dept Breast Canc, Harbin, Peoples R China
[2] Harbin Med Univ, Canc Hosp, Tumor Biobank, Harbin, Peoples R China
[3] Heilongjiang Acad Med Sci, Harbin 150086, Peoples R China
[4] Heilongjiang Acad Med Sci, Sinorussian Med Res Ctr, Harbin, Peoples R China
[5] Heilongjiang Acad Med Sci, Northern China Translat Med Res & Cooperat Ctr, Harbin, Peoples R China
来源：
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2015年 / 8卷 / 05期
关键词：
Long noncoding RNA; MALAT1; EMT; metastasis; breast cancer; EXPRESSION; METASTASIS; GRADE; STAGE;
D O I：
暂无
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
The metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) regulates cell motility via the transcriptional or post-transcriptional control of motility-related genes. Whether MALAT1 plays a critical role in cancer progression in breast cancer remains unclear. In this study, we found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways. Furthermore, lower expression of MALAT1 in breast cancer patients was associated with shorter relapse-free survival. Thus, our results indicate for the first time that MALAT1 is a novel regulator of EMT in breast cancer and may be a potential therapeutic target for breast cancer metastasis.
引用
收藏
页码：4881 / U2358
页数：12
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