已发表论文

MiR-29a 通过靶向 SIRT1 在宫颈癌中发挥肿瘤抑制作用,并可预测患者预后

 

Authors Nan P, Niu Y, Wang X, Li Q

Received 2 June 2019

Accepted for publication 31 July 2019

Published 26 August 2019 Volume 2019:12 Pages 6917—6925

DOI https://doi.org/10.2147/OTT.S218043

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Shreya Arora

Peer reviewer comments 2

Editor who approved publication: Dr Leo Jen-Liang Su

Introduction: Cervical cancer is the second most frequently malignant tumors in females and metastasis is a challenge of the treatment of cervical cancer. MiR-29a is usually low expressed in several tumors and its functions in cervical cancer remain unclear.
Patients and methods: The quantitative real-time polymerase chain reaction was employed to assess the expression of miR-29a and the Sirtuin-1 (SIRT1). Cell metastatic ability was assessed using Transwell and Western blot assays. The dual-luciferase reporter assay was performed to verify that miR-29a targeted to the 3’-untranslated region (UTR) of SIRT1 mRNA.
Results: MiR-29a was low expressed in cervical cancer and downregulation of miR-29a was associated with poor outcome. MiR-29a regulated the expression of SIRT1 by targeting to its 3’-UTR of mRNA in HeLa cells. SIRT1 was upregulated in cervical cancer tissues and cells in comparison with the non-tumor tissues and normal cells. Upregulation of SIRT1 predicted worse outcome of cervical cancer patients. MiR-29a was participated in the migration, invasion and epithelial–mesenchymal transition (EMT) in cervical cancer through directly targeting to the 3’-UTR of SIRT1 mRNA. SIRT1 reversed partial roles of miR-29a on metastasis in cervical cancer.
Conclusion: miR-29a suppressed migration, invasion and EMT by directly targeting to SIRT1 in cervical cancer. The newly identified miR-29a/SIRT1 axis provides novel insight into the pathogenesis of cervical cancer.
Keywords: miR-29a, cervical cancer, SIRT1, tumor suppressor, EMT




Figure 3 miR-29a regulated the expression of SIRT1 through directly binding to the 3’-UTR of its mRNA...