Journal
NEOPLASMA
Volume 67, Issue 3, Pages 528-+Publisher
AEPRESS SRO
DOI: 10.4149/neo_2020_190703N582
Keywords
miR-769-5p; JAK1/STAT3 pathway; oral squamous cell carcinoma
Categories
Funding
- Joint Project of Cangzhou-Southwest Medical University: Youth Innovation Team of Orthodontic Tooth Movement Mechanism [:2016LZXNYD-T04]
- Basic Research on the Application of Cangzhou Science and Technology and Talents Bureau [2018-JYJ-37]
Ask authors/readers for more resources
Oral squamous cell carcinoma (OSCC) is the most common human malignancy worldwide with a high mortality rate. MiR-769-5p has been reported to be downregulated in tissues and blood of OSCC patients. However, the exact roles and pathogenesis of miR-769-5p involved in OSCC remain unclear. The expressions of miR-769-5p and Janus kinase (JAK1) in OSCC tissues and cells were assessed by RT-qPCR and western blot assay. Expressions of apoptotic-related (Bcl-2, Bax, and cleaved-caspase 3) and EMT-associated proteins (MMP9, E-cadherin, N-cadherin, and Vimentin) were detected by western blot assay. The effect of miR-769-5p and JAK1 on proliferation, migration, invasion, and apoptosis was evaluated by CCK-8, transwell, and flow cytometry assays, respectively. The binding interaction of miR-769-5p and JAK1 were predicted by TargetScan and demonstrated by dual-luciferase reporter assays. The volume and weight of the tumor were measured in the subcutaneous transplantation experiment. MiR-769-5p was downregulated, and JAK1 was upregulated in OSCC tissues and cells. MIR-769-5p restrained Bcl-2, MMP9, N-cadherin, and Vimentin protein level and accelerated Bax, cleaved-caspase 3 and E-cadherin protein level, while JAK1 partly overturned these effects. Also, miR-769-5p suppressed proliferation, migration, invasion, and increased apoptosis of OSCC, while the reintroduction of JAK1 abolished these effects. Moreover, JAK1 was verified to be the target of miR-769-5p. In addition, miR-769-5p inhibited the development of OSCC cells in vivo. These results indicate that miR-769-5p suppressed OSCC cell development via targeting the JAK1/STAT3 pathway, providing an underlying therapeutic method for OSCC.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available