期刊
ORAL DISEASES
卷 20, 期 3, 页码 e65-e75出版社
WILEY
DOI: 10.1111/odi.12133
关键词
phosphatase; miR-99a; oral cancer; MTMR3; microRNA
资金
- National Science Council [98-2320-B-006-034-MY3, 99-2628-B-006-017-MY3, 101-2325-B-006-005]
- Department of Health [DOH-101-TD-C-111-003]
- Department of Health, Executive Yuan in Taiwan [DOH100-TD-C-111-003]
- National Core Facility Program for Biotechnology Grant [NSC 100-2319-B-001-002]
Objective We aimed at studying the role of the most deregulated miR-99a, identifying its downstream targets, and exploring the clinical potential of miR-99a and its target(s) in oral cancer. Subjects and Methods Following confirmation of miR-99a deregulation in nine oral lines and 26 pairwise clinical specimens, miR-99a-manipulated oral cancer cells were subjected to cell proliferation, migration, invasion, and in vivo murine metastasis assays. We characterized putative miR-99a target(s) using luciferase reporter assays and genetic manipulation. The inverse relation of miR-99a and its target(s) was examined in clinical specimens using real-time PCR and Western blot analysis. Results MiR-99a down-regulation was confirmed both in tested oral cancer cell lines and clinical specimens. Ectopic miR-99a expression inhibited oral cancer cell migration and invasion. Anti-miR-99a, silencing miR-99a functions, had the opposite effect. Myotubularin-related protein 3 (MTMR3) with one evolutionarily conserved seed region in the 3 '-untranslated region was a novel miR-99a target. Depleting MTMR3 expression significantly reduced cell proliferation, migration, or invasion. There was an inverse expression of miR-99a and MTMR3 protein in oral cancer lines and clinical specimens. Conclusion miR-99a repressed oral cancer cell migration and invasion partly through decreasing MTMR3 expression. MTMR3 may serve as a therapeutic target for oral cancer treatment.
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