J Cancer 2020; 11(8):2201-2212. doi:10.7150/jca.40319 This issue

Research Paper

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Wu Wu1, Li Guo2, Zhenlong Liang3, Yuanbin Liu4✉, Zhi Yao1✉

1. Department of Immunology, Tianjin Key Laboratory of Cellular and Molecular Immunology, Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin 300051, China.
2. Department of Clinical Laboratory, Laigang Hospital, Jinan 271103, China.
3. Department of Clinical Laboratory, Chinese PLA General Hospital, Beijing 100853, China.
4. Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan 250002, China.

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Wu W, Guo L, Liang Z, Liu Y, Yao Z. Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells. J Cancer 2020; 11(8):2201-2212. doi:10.7150/jca.40319. Available from https://www.jcancer.org/v11p2201.htm

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Background: The lnc-SNHG16 serves as an oncogene and miR-128 acts as a tumor suppressor in various cancers. However, the functional role of lnc-SNHG16 and miR-128 in CC still remain unknown. This study aims to explore the expression level of lnc-SNHG16 and miR-128 and its biological roles in CC.

Methods: lnc-SNHG16, miR-128, GSPT1 and WNT3A expression were analyzed using quantitative real-time PCR and bioinformatics in cervical cancer tissues and cells. Cell Counting Kit-8, EdU staining, colony formation assay, western blot, Transwell, immunofluorescence, immunohistochemical staining, luciferase reporter assay, electrophoretic mobility shift, tumor xenograft, and flow cytometry assays were employed to investigate the mechanisms underlying the effect of Lnc-SNHG16/miR-128 axis on cervical cancer.

Results: lnc-SNHG16 was up-regulated in CC cell lines and tissues. lnc-SNHG16 knockdown inhibited proliferation, restrained the epithelial-mesenchymal transition (EMT) process by regulating cell apoptosis and cell cycle. The next study indicated that lnc-SNHG16 knockdown markedly increased miR-128 level which is down-regulated in CC. Moreover, miR-128 overexpression significantly inhibited proliferation, EMT process and tumor growth by directly targeting GSPT1 and WNT3A. Finally, lnc-SNHG16 activates but miR-128 inactivates the WNT/β-catenin pathways in CC cells.

Conclusion: Our data suggest that lnc-SNHG16/miR-128 axis modulates malignant phenotype of CC cells through WNT/β-catenin pathway.

Keywords: lnc-SNHG16, miR-128, GSPT1, WNT3A, WNT/β-catenin, cervical cancer