To investigate the molecular mechanisms of S-adenosine methionine in suppressing lung cancer metastasis with a miRNA-34a-dependent manner.

A549 lung cancer cell was selected as the study model of this time research. A549 cells were stimulated with 0, 50, 100, 200, 500 μM SAMe, respectively and the expression of miR-34a and its related STAT3 signaling pathways were also detected. The invasive capacity of cells was detected under various condition as well; miR-34a, E-cadherin, α-catenin, N-cadherin and Vimentin mRNA expression were detected by qPCR method; Western Blot was used to detect expression of STAT3, p-STAT3 and β-actin; Invasive capacity of A549 cells was detected by Transwell experiment.

As the increase of SAMe concentration, miR-34a expression increased gradually, and when it was compared to the control group, the difference was statistically significant through the t-test (P<0.05); Western Blot experiments showed that p-STAT3 protein level of 500 μM SAMe stimulation was lower than 0 μM treatment, while total STAT3 and β-actin level had no change; q-PCR results showed that E-cadherin and α-catenin level elevated, but N-cadherin and Vimentin level decreased as the increase of drug concentration; Transwell experiments showed that invasive inhibitory rates of A549 cells in 50, 100, 200, 500 μM of SAMe were 18.70%, 31.24%, 47.66% and 58.46%, respectively. And compared to the control group, the difference had statistical significance by t-tset (P<0.05).

SAMe could suppress cell metastasis through a miR-34a-dependent manner by inhibiting STAT3 signaling pathway in lung cancer cells, which suggested a potential role of SAMe in metastasis of lung cancer.