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

Abstract	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.
Authors	Shouping Xu, Shiyao Sui, Jinfeng Zhang, Nanxia Bai, Qingyu Shi, Guangwen Zhang, Song Gao, Zilong You, Chao Zhan, Feng Liu, Da Pang
Journal	International journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 8 Issue 5 Pg. 4881-91 ( 2015) ISSN: 1936-2625 [Electronic] United States
PMID	26191181 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	MALAT1 long non-coding RNA, human RNA, Long Noncoding Phosphatidylinositol 3-Kinase Proto-Oncogene Proteins c-akt
Topics	Breast Neoplasms (enzymology, genetics, pathology) Disease-Free Survival Down-Regulation Epithelial-Mesenchymal Transition Female Gene Expression Regulation, Neoplastic Humans Kaplan-Meier Estimate Lymphatic Metastasis MCF-7 Cells Middle Aged Neoplasm Recurrence, Local Phosphatidylinositol 3-Kinase (metabolism) Prognosis Proto-Oncogene Proteins c-akt (metabolism) RNA Interference RNA, Long Noncoding (genetics, metabolism) Risk Factors Signal Transduction Time Factors Transfection

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