Studies on the regulatory role of microRNA-30d in chrysotile-transformed MeT-5A cells.

Abstract

Asbestos is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC) because of its propensity to accumulate in the lungs and induce malignant tumors, including lung cancer and malignant mesothelioma. The objective of this study was to examine the inhibitory impact of miR-30d on the proliferation, migration, and invasion of chrysotile-transformed human pleural mesothelial cells (MeT-5A). The asbestos-transformed cell model was constructed using a chrysotile asbestos chronically exposed human pleural mesothelial cell line (MeT-5A). The expression level of miR-30d in the transfected cells was determined by qRT-PCR. Cell viability was assessed by CCK-8 assay. The apoptosis rate was evaluated by flow cytometry. The cell scratch assay and the Transwell assay were used to assess cell migration and invasion ability. It was observed that the expression level of miR-30d in Asb MeT-5A+miR-30d cells transfected with miR-30d mimics was markedly elevated in comparison to that in Asb MeT-5A+miR NC cells. Additionally, the cell viability in Asb MeT-5A+miR-30d cells was significantly diminished, while the level of apoptosis was markedly elevated in comparison to that in Asb MeT-5A+miR NC cells. The relative migration area was significantly lower in the Asb MeT-5A+miR-30d group than in the Asb MeT-5A+miR NC group. Furthermore, the number of migrated and invaded cells in the Asb MeT-5A+miR-30d group was significantly less than in the Asb MeT-5A+miR NC group. The findings suggest that miR-30d may suppress the proliferation, apoptosis, migration, and invasion of chrysotile-transformed pleural mesothelial cells.