MiR-17 Regulates Prostate Cancer Cell Proliferation and Apoptosis Through Inhibiting JAK-STAT3 Signaling Pathway

STAT3 is an important protein in Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway that facilitates B-cell lymphoma 2 (Bcl-2) expression. MiR-17 was found to be significantly reduced in prostate cancer tissues and cells, suggesting that it might be a tumor suppressor in prostate cancer tumorigenesis. Bioinformatics analysis showed the complementary binding site between miR-17 and STAT3. This study aimed to investigate the role of miR-17 in regulating JAK-STAT signaling pathway, as well as prostate cancer cell proliferation and apoptosis.

Dual luciferase assay was used to verify the targeted relationship between miR-155 and STAT3. LNCaP cells were cultured in vitro and divided into four groups, including mimic NC, miR-17 mimic, si-NC, and si-STAT3 groups. STAT3, p-STAT3, and Bcl-2 expressions were tested by western blot. Cell apoptosis was detected by flow cytometry. Cell proliferation was assessed by EdU staining.

MiR-17 mimic transfection significantly reduced the relative luciferase activity in HEK293T cells. MiR-17 targeted regulated STAT3 expression. MiR-17 expression and cell apoptosis were obviously declined, while STAT3 level and cell proliferation markedly were elevated in LNCaP cells compared with RWPE-1 cells. MiR-17 mimic and/or si-STAT3 transfection significantly downregulated the expression of STAT3, p-STAT3, and Bcl-2, attenuated cell proliferation, and enhanced cell apoptosis in LNCaP cells.

Upregulation of miR-17 inhibited LNCaP cell proliferation and induced cell apoptosis by downregulating the expression of STAT3, p-STAT3, and Bcl-2.