Keyong Bao,1 Xue Zhang,1 Lihong Bao,2 Xiaoyu Tao,1 Li Zhang,1 Dong Wang3 

1Department of Gynecology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, 028000, People’s Republic of China; 2Prevention College of Inner Mongolia University for Nationalities, Tongliao, Inner Mongolia, 028000, People’s Republic of China; 3Department of Oncology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, 028000, People’s Republic of China

Correspondence: Dong Wang, Department of oncology, Affiliated Hospital of Inner Mongolia University for the Nationalities, 1742, Huolinhe Street, Tongliao, Inner Mongolia, 028000, People’s Republic of China, Email wangdong123567@163.com

Background: This study aimed to investigate the function of miR-484 in C33A cells, as well as its mechanism.
Methods: The mRNA expression patterns of miR-484 and Krüppel-like factor 12 (KLF12) in C33A cells were detected by quantitative reverse transcription polymerase chain reaction. MiR-484 mimics and miR-484 negative controls were transfected into C33A cells. Luciferase reporter assay was used to confirm the binding of miR-484 and KLF12. The effects of miR-484 on cell viability, migration, invasion, and apoptosis were assessed using the cell counting kit-8 assay, wound healing assay, Transwell assay, flow cytometry, and Western blot. Rescue experiments were performed by overexpressing KLF12. Western blot was utilized to examine the expression of KLF12, interleukin-6 (IL-6), Janus Kinase 2, phosphorylated-Janus Kinase 2, signal transducer and activator of transcription 3 (STAT3), and phosphorylated-STAT3 proteins.
Results: MiR-484 expression was down-regulated in C33A cells, while KLF12 was up-regulated. The luciferase reporter assay confirmed the direct binding of miR-484 to KLF12. MiR-484 inhibited the proliferation, migration, and invasion of C33A cells while promoting apoptosis. Additionally, it could inhibit the expression of KLF12 protein and the activation of the IL-6/STAT3 signaling pathway. However, KLF12 overexpression could reverse the above effects.
Conclusion: MiR-484 can specifically inhibit the KLF12-mediated IL-6/STAT3 signaling pathway, thereby suppressing the malignant biological behavior of C33A cells.

Keywords: cervical cancer, miR-484, KLF12, IL-6/STAT3 signaling pathway