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miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.

Feng, Tongbao; Shao, Fang; Wu, Qiyong; Zhang, Xiaohang; Xu, Dongqin; Qian, Keqing; Xie, Yewen; Wang, Shizhong; Xu, Ning LU and Wang, Yong, et al. (2016) In Oncotarget 7(13). p.16205-16216
Abstract
The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recently shown to be dysregulated in several cancers. However, the mechanisms underlying the role of MALAT1 in breast cancer remain unclear. Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells. MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo. Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. Taken... (More)
The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recently shown to be dysregulated in several cancers. However, the mechanisms underlying the role of MALAT1 in breast cancer remain unclear. Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells. MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo. Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. Taken together, our data highlight the pivotal role of MALAT1 in breast cancer tumorigenesis. Moreover, the present study elucidated the MALAT1-miR-124-CDK4/E2F1 signaling pathway in breast cancer, which might provide a new approach for tackling breast cancer. (Less)
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published
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Oncotarget
volume
7
issue
13
pages
16205 - 16216
publisher
Impact Journals, LLC
external identifiers
  • PMID:26918449
  • Scopus:84971646911
ISSN
1949-2553
DOI
10.18632/oncotarget.7578
language
English
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yes
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b0f580d2-e391-4dca-9bb8-979b05c0d54e (old id 8821557)
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http://www.ncbi.nlm.nih.gov/pubmed/26918449?dopt=Abstract
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2016-03-03 13:38:46
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2016-11-13 04:27:26
@misc{b0f580d2-e391-4dca-9bb8-979b05c0d54e,
  abstract     = {The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recently shown to be dysregulated in several cancers. However, the mechanisms underlying the role of MALAT1 in breast cancer remain unclear. Herein, we showed that MALAT1 was aberrantly increased in breast cancer tissues and cells. MALAT1-siRNA inhibited breast cancer cell proliferation and cell cycle progression in vitro and in vivo. Furthermore, MALAT1 acted as an endogenous potent regulator by directly binding to miR-124 and down-regulating miR-124 expression. In addition, MALAT1 reversed the inhibitory effect of miR-124 on breast cancer proliferation and was involved in the cyclin-dependent kinase 4 (CDK4) expression. Taken together, our data highlight the pivotal role of MALAT1 in breast cancer tumorigenesis. Moreover, the present study elucidated the MALAT1-miR-124-CDK4/E2F1 signaling pathway in breast cancer, which might provide a new approach for tackling breast cancer.},
  author       = {Feng, Tongbao and Shao, Fang and Wu, Qiyong and Zhang, Xiaohang and Xu, Dongqin and Qian, Keqing and Xie, Yewen and Wang, Shizhong and Xu, Ning and Wang, Yong and Qi, Chunjian},
  issn         = {1949-2553},
  language     = {eng},
  month        = {02},
  number       = {13},
  pages        = {16205--16216},
  publisher    = {ARRAY(0x8d9bfe8)},
  series       = {Oncotarget},
  title        = {miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.},
  url          = {http://dx.doi.org/10.18632/oncotarget.7578},
  volume       = {7},
  year         = {2016},
}