LKB 1 regulates JAK 2 / STAT 3 pathways involved in apoptosis of prostate cancer PC-3 cells

Objective: The aim of this study was to investigate the effects of LKB1 on apoptosis of prostate cancer cells, examining its mechanisms. Methods: Prostate cancer PC-3 cells were transfected with LKB1 overexpression vectors (PC-3-LBK1 overexpression group) and negative controls (PC-3-vector group). Normal human prostate cells were used as control A group and untreated PC-3 cells were used as control B group. Relative expression levels of LKB1 genes were detected by quantitative real-time-PCR. Western blotting was conducted to detect relative protein expression levels of JAK2, STAT3, phosphorylated JAK2 (p-JAK2), and phosphorylated STAT3 (p-STAT3). Flow cytometry was conducted to detect apoptosis. Spearman’s analysis was used to explore the correlation between relative expression levels of LKB1 genes and p-JAK2 and p-STAT3 proteins in PC-3 cells. Results: After PC-3 cells were transfected into LKB1 overexpression vectors, relative expression levels of LKB1 genes, LKB1 proteins, and p-JAK2 and p-STAT3 proteins in the PC-3-LBK1 overexpression group were significantly higher than those in the PC-3-vector group (P<0.05). An increase in LKB1 gene expression levels promoted PC-3 cell proliferation. Cell viability in the PC-3-vector group and PC-3-LBK1 overexpression group increased continuously over time (P<0.05). Cell viability in the PC-3-LBK1 overexpression group was lower than that in the PC-3-vector group. (P<0.05). An increase in LKB1 gene expression levels decreased apoptosis rates of PC-3 cells in the PC-3-vector group, normal human prostate cells group, and PC-3 cells group. Spearman’s correlation analysis showed that LKB1, p-JAK2 (r=0.984, P<0.001), and p-STAT3 (r=0.988, P<0.001) were positively related. Conclusion: LKB1 may promote apoptosis of prostate cancer cells by activating JAK2/STAT3 signal pathways and inhibiting cancer, making this protein a potential target for treatment of prostate cancer.