Abstract |
Our previous high-throughput sequencing indicated that rno-miR-1298 was down-regulated in ischemia-reperfusion model of rat. However, little is known about the function and molecular mechanism of rno-miR-1298 in rat tumor cell. In this study, rno-miR-1298 was detected to be significantly down-regulated in rat tumor C6 cells. Moreover, overexpression of rno-miR-1298 obviously inhibited the proliferation and induced apoptosis in C6 cells. SET domain containing 7 (SETD 7) was identified to be a target of rno-miR-1298 using bioinformatics and luciferase reporter assays. Overexpression of rno-miR-1298 markedly reduced the expression of SETD 7 at protein level. Knockdown of SETD 7 also suppressed proliferation and promoted apoptosis in C6 cells. It was indicated that rno-miR-1298 affected cell proliferation and apoptosis of rat tumor cells by targeting SETD 7. Thus, the newly identified miR-1298/SETD 7 expands the elaboration of the mechanisms of the development and progression of tumors and may provide therapeutic target for tumors of nervous system.
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Authors | Chun-Mei Wang, Bao-Hua Cheng, Qing-Jie Xue, Jing Chen, Bo Bai |
Journal | International journal of immunopathology and pharmacology
(Int J Immunopathol Pharmacol)
Vol. 30
Issue 3
Pg. 264-271
(Sep 2017)
ISSN: 2058-7384 [Electronic] England |
PMID | 28762861
(Publication Type: Journal Article)
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Chemical References |
- MIRN1298 microRNA, rat
- MicroRNAs
- Histone-Lysine N-Methyltransferase
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Topics |
- Animals
- Apoptosis
- Cell Line, Tumor
- Cell Proliferation
- Down-Regulation
- Histone-Lysine N-Methyltransferase
(genetics, metabolism)
- MicroRNAs
(genetics)
- Rats
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