Abstract |
Long non-coding RNA LOXL1-AS is up-regulated in several types of cancers. The present study was carried out to explore the potential interactions between LOXL1-AS and lncRNA Giver in thoracic aortic aneurysm (TAA). We found that LOXL1-AS was up-regulated in TAA patients than in healthy controls in aortic media specimens. Altered expression levels of LOXL1-AS distinguished TAA patients from healthy controls. LncRNA Giver was also up-regulated in TAA patients than in healthy controls in aortic media specimens, and was positively correlated with LOXL1-AS. LOXL1-AS overexpression mediated the up-regulation of Giver in human aortic smooth muscle cells, while Giver overexpression failed to significantly affect LOXL1-AS. LOXL1-AS and Giver overexpression resulted in promoted proliferation and inhibited apoptosis of HAOSMC. Giver silencing played an opposite role and attenuated the effect of LOXL1-AS overexpression. Therefore, LOXL1-AS was up-regulated in TAA and regulated proliferation and apoptosis of LOXL1-AS by up-regulating Giver.
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Authors | Ben Huang, Shuyang Lu, Hao Lai, Jun Li, Yongxin Sun, Chunsheng Wang |
Journal | Bioscience reports
(Biosci Rep)
Vol. 39
Issue 9
(09 30 2019)
ISSN: 1573-4935 [Electronic] England |
PMID | 31471532
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2019 The Author(s). |
Chemical References |
- RNA, Long Noncoding
- Amino Acid Oxidoreductases
- LOXL1 protein, human
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Topics |
- Adult
- Amino Acid Oxidoreductases
(genetics)
- Aorta
(metabolism, pathology)
- Aortic Aneurysm, Thoracic
(genetics, pathology)
- Apoptosis
(genetics)
- Cell Proliferation
(genetics)
- Cells, Cultured
- Female
- Gene Expression Regulation
(genetics)
- Humans
- Male
- Middle Aged
- Myocytes, Smooth Muscle
(metabolism, pathology)
- RNA, Long Noncoding
(genetics)
- Transcriptional Activation
(genetics)
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