Objective: JAK2 expression and dysfunction play a role in tumor pathogenesis. Bioinformatics analysis revealed a targeted binding site between miR-101 and the 3'-UTR of JAK2 mRNA. This study investigated the role of miR-101 in regulating JAK2 expression and affecting the proliferation and apoptosis of cervical cancer cells.
Patients and methods: The tumor tissues and adjacent tissues of patients with cervical cancer were collected. The expression of miR-101 and JAK2 was detected by qRT-PCR. The dual luciferase reporter gene assay validated the targeting relationship between miR-101 and JAK2. The cervical cancer Caski cells were cultured in vitro, and divided into miR-NC group and miR-101 mimic group. The expression of JAK2 and p-JAK2 was detected by Western blot, cell apoptosis was detected by flow cytometry, and cell proliferation was detected by EdU staining.
Results: Compared with adjacent tissues, miR-101 expression was significantly decreased, and JAK2 expression was increased in cervical cancer tissues. There was a targeted regulatory relationship between miR-101 and JAK2. Compared with HcerEpic cells, miR-101 expression in HeLa and Caski was significantly decreased, and the expression of JAK2 and p-JAK2 was significantly increased. Transfection of miR-101 mimic significantly reduced the expression of JAK2 and p-JAK2 in Caski cells, reduced cell proliferation and increased cell apoptosis.
Conclusions: The decrease of miR-101 expression and the increase of JAK2 expression play a role in cervical cancer, while the increase of miR-101 expression can inhibit the proliferation and promote the apoptosis of cells by inhibiting the expression of JAK2.