Long non-coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p
Autor: | Shuyuan Wang, Ximei Zhang, Jing Lin, Shunheng Zhou, Qingyuan Zhang, Weiguang Yuan, Huilong Cai, Lihong Wang, Yan Song, Tian Luan, Yue Yang, Weiwei An |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Metastasis miR-155 03 medical and health sciences breast cancer Breast cancer Downregulation and upregulation medicine miR-155-5p skin and connective tissue diseases Gene knockdown Competing endogenous RNA business.industry ceRNA medicine.disease MIAT Long non-coding RNA Surgery 030104 developmental biology Oncology DUSP7 Apoptosis Cancer research business Research Paper |
Zdroj: | Oncotarget |
ISSN: | 1949-2553 |
DOI: | 10.18632/oncotarget.19190 |
Popis: | Long non-coding RNAs (lncRNA) have been reported as key regulators in the progression and metastasis of breast cancer. In this study, we found that the lncRNA myocardial infarction associated transcript (MIAT) expression was upregulated in breast cancer in The Cancer Genome Atlas (TCGA) data sets. We validated that MIAT was higher in breast cancer cell lines and advanced breast tumors than in normal controls. And MIAT overexpression associated with TNM stage and lymphnode metastasis. Knockdown MIAT inhibited breast cancer cell proliferation and promoted apoptosis. Also MIAT downregulation suppressed epithelial-mesenchymal transition (EMT) and decreased migration and invasion in MDA-MB-231 and MCF-7 breast cancer cell lines. More importantly, knockdown MIAT inhibited tumor growth in vivo. Our results suggested that MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients. We conclude that MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. |
Databáze: | OpenAIRE |
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