Objective To explore the effect of L-mimosine on proliferation, migration and invasion of lung cancer cells and its possible mechanism.

Methods Low dose, medium dose, high dose (100, 200, 400 μmol/L) of L-mimosine were used to treat human A549 cells of lung cancer. The Methyl Thiazolyl Tetrazolium (MTT) method, plate colony formation experiment, scratch assay, Transwell assay and western blotting were used to detect cell proliferation, migration and invasion ability. The quantitative real-time polymerase chain reaction(qRT-PCR) was used to detect the expression of micrornA-1301-3p (miR-1301-3p) in lung cancer A549 cells and human normal lung epithelial cells BEAS-2B. Anti-miR-NC and anti-miR-1301-3p were respectively transfected into A549 cells, and the mimics of miR-NC and miR-1301-3p were transfected into A549 cells and treated with L-mimosine for 24 h. Their cell phenotypes were analyzed respectively.

Results With the increase of L-mimosine dose, the proliferation inhibition rate and E-cadherin protein level of A549 cells were increased, while the expression level of miR-1301-3p, scratch healing rate, N-cadherin protein level, the number of cell clonal formation and the number of invasion cell were decreased (P < 0.05). The expression of miR-1301-3p in A549 cells was higher than that in BEAS-2B cells (P < 0.05). Compared with transfection with anti-miR-NC, the proliferation inhibition rate and E-cadherin protein level of cells transfected with anti-miR-1301-3p were increased, while the number of cell clone formation, the number of invasive cells, scratch healing rate and N-cadherin protein level were decreased (P < 0.05). Compared with transfection with L-mimosine+miR-NC, cells transfected with L-mimosine+miR-1301-3p mimics had reduced cell proliferation inhibition rate and E-cadherin protein level, and had increased the number of cell clone formation, the number of invasion cell, scratch healing rate and N-cadherin protein level (P < 0.05).

Conclusion L-mimosine could inhibit the proliferation, migration and invasion of lung cancer cells, and its mechanism may be related to the down-regulation of miR-1301-3p expression.