MiR-101 affects proliferation and apoptosis of cervical cancer cells by inhibition of JAK2.

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.