BACKGROUND: This study aimed to explain the effects and mechanism of MT1JP in lung cancer development and treatment.

MATERIAL AND METHODS: Thirty non-small cell lung cancer (NSCLC) (stages I–II, 17 cases; stages III–IV, 13 cases) and adjacent normal tissues were obtained. MT1JP and miRNA-423-3p levels were assessed by in situ hybridization and Bim protein expression by immunohistochemistry, and the correlations determined were analyzed. Cell proliferation was determined using MTT and colony formation assay, and cell apoptosis was measured using flow cytometry. A549 cell invasion and migration were assessed by Transwell migration and scratch wound healing assays. Relative mRNA and protein expressions were assessed using real-time polymerase chain reaction and western blotting. Correlations between miRNA-423-3p and Bim protein were investigated using luciferase activity assay, and Bim protein expression was evaluated using western blotting.

RESULTS: MT1JP, miRNA-423-3p, and Bim expressions in NSCLC cancer tissues and those in adjacent cancer tissues were significantly different (P<0.01 or P<0.001) with increasing stage. Compared with those in the normal control (NC) group, cell proliferation rates were significantly suppressed (P<0.01 or P<0.001) and cell apoptosis rates significantly increased (P<0.01 or P<0.001) in the miRNA inhibitor and lncRNA+miRNA inhibitor groups. Invasion cell numbers and wound healing rates were also significantly inhibited in the miRNA inhibitor and lncRNA+miRNA inhibitor groups (P<0.01 or P<0.001) compared with those in the NC group.

CONCLUSIONS: The lncRNA MT1JP suppresses NSCLC biological activities by regulating the miRNA-423-3p/Bim axis.

Keywords: ankle fractures, A549 cells, Bcl-2-Like Protein 11, metallothionein