Moreover, miR-32*, miR-466i-5p, and mmu-miR-669c in SP<sup>+</sup> lung cancer stem cells were confirmed, as well as mmu-miR-106b*, mmu-miR-144, mmu-miR-669k*, mmu-miR-142-3p, mmu-miR-210, and mmu-miR-223 in CD34<sup>+</sup>SCA1<sup>+</sup> bone marrow hematopoietic stem cells.
Thus, these findings indicate that PM2.5 can induce the EMT process through the Smad1-mediated signaling pathway, and miR-32 may act as an EMT inhibitor in lung cancer cells.
The online bioinformatic tool RNAhybrid revealed that linc00319 potentially bound with the miR-32, which functioned as a tumor suppressor in lung cancer.
The expression of miR-32 was significantly decreased in lung cancer cell lines and NSCLC tissues compared with normal bronchial epithelial cells and adjacent non-tumor tissues (P < 0.05).