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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-1298 affects cell proliferation and apoptosis in C6 cells by targeting SET domain containing 7
Chun-Mei Wang1, Bao-Hua Cheng1, Qing-Jie Xue1
1Neurobiology Institute, Jining Medical University, Jining, P.R. China.
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.
Insights
Rattumor cells show decreased levels of microRNA-1298 (miR-1298). Restoring miR-1298 inhibits tumor cell growth and promotes cell death by targeting SET domain containing 7 (SETD7).
Area of Science:
- Molecular Biology
- Oncology
- Neuroscience
Background:
- MicroRNAs (miRNAs) play crucial roles in cellular processes, including tumor development.
- Previous studies indicated down-regulation of rno-miR-1298 in a rat ischemia-reperfusion model.
- The specific function and molecular mechanisms of rno-miR-1298 in rat tumor cells remain largely unexplored.
Purpose of the Study:
- To investigate the role of rno-miR-1298 in rat C6 glioma cells.
- To identify the molecular targets and mechanisms underlying rno-miR-1298's function in tumor progression.
Main Methods:
- Quantitative analysis of rno-miR-1298 expression in C6 cells.
- Overexpression and knockdown experiments to assess functional impacts.
- Bioinformatics analysis and luciferase reporter assays to identify miRNA targets.
- Western blot analysis to confirm target protein regulation.
Main Results:
- Rno-miR-1298 was significantly down-regulated in rat C6 tumor cells.
- Overexpression of rno-miR-1298 inhibited C6 cell proliferation and induced apoptosis.
- SET domain containing 7 (SETD7) was validated as a direct target of rno-miR-1298.
- Knockdown of SETD7 mimicked the effects of rno-miR-1298 overexpression, suppressing proliferation and promoting apoptosis.
Conclusions:
- Rno-miR-1298 suppresses proliferation and induces apoptosis in rat glioma cells by targeting SETD7.
- The miR-1298/SETD7 axis represents a novel regulatory pathway in tumor development.
- This pathway offers potential therapeutic targets for nervous system tumors.
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