期刊
CHINESE MEDICAL JOURNAL
卷 134, 期 5, 页码 564-572出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/CM9.0000000000001400
关键词
miR-296-5p; Osteosarcoma; SND1; Tumor suppressor; miRNA
资金
- National Natural Science Foundation of China [81572179, 81874018]
- Clinical Special Program of Jiangsu Province [BL2014044]
- Mingsheng Science andTechnology Project of Suzhou City [SS201634, SS201814]
- Clinical Medical Center Project of Suzhou City [SZZX201504]
- Advantage Discipline Groups of the Second Affiliated Hospital of Soochow University [XKQ2015001]
- Zhejiang Provincial Natural Science Foundation of China [LY15H060006, LY16H060007]
- Zhejiang Provincial Health Bureau Science Foundation of China [2018KY017]
The study revealed that miR-296-5p acts as a tumor suppressor in OS by targeting SND1, providing a potential novel therapeutic target for OS treatment.
Background: The pathogenesis of osteosarcoma (OS) is still unclear, and it is still necessary to find new targets and drugs for anti-OS. This study aimed to investigate the role and mechanism of the anti-OS effects of miR-296-5p. Methods: We measured the expression of miR-296-5p in human OS cell lines and tissues. The effect of miR-296-5p and its target gene staphylococcal nuclease and tudor domain containing 1 on proliferation, migration, and invasion of human OS lines was examined. The Student's t test was used for statistical analysis. Results: We found that microRNA (miR)-296-5p was significantly downregulated in OS cell lines and tissues (control vs. OS, 1.802 +/- 0.313 vs. 0.618 +/- 0.235, t = 6.402, P < 0.01). Overexpression of miR-296-5p suppressed proliferation, migration, and invasion of OA cells. SND1 was identified as a target of miR-296-5p by bioinformatic analysis and dual-luciferase reporter assay. Overexpression of SND1 abrogated the effects induced by miR-296-5p upregulation (miRNA-296-5p vs. miRNA-296-5p + SND1, 0.294 +/- 0.159 vs. 2.300 +/- 0.277, t = 12.68, P = 0.003). Conclusion: Our study indicates that miR-296-5p may function as a tumor suppressor by targeting SND1 in OS.
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