Add time:07/27/2019         Source:sciencedirect.com

In the present study, we investigated the proteomic profiling of anti-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (anti-BPDE)-transformed human bronchial epithelial cell line (16HBE-C) and its parental cell line (16HBE) G0/G1 cells. Differential analysis of proteomic profiling indicated that 67 polypeptides were down-regulated and 77 polypeptides were up-regulated in 16HBE-C G0/G1 cells compared to 16HBE G0/G1 cells. Then 16 differentially expressed protein spots were analyzed with Q-TOF MS/MS. Of these spots, 3 down-regulated polypeptides were identified as sorcin, small ubiquitin-related modifier 2 precursor and eukaryotic translation initiation factor 5A-1, and 9 up-regulated polypeptides were identified as calmodulin, myosin light polypeptide 6, eukaryotic translation initiation factor 6, proliferating cell nuclear antigen (PCNA), tumor protein D52 (TPD52), superoxide dismutase [Cu-Zn], prohibitin, nuclear protein Hcc-1 and vimentin. These proteins are involved in cell proliferation, protein synthesis, signal transduction and carcinogenesis. Western blotting analysis verified the increased expression levels of PCNA and TPD52 in 16HBE-C G0/G1 cells. Based on the clues from proteomic analysis, the migration and invasion capabilities of 16HBE-C and 16HBE cells were tested. The results indicated that 16HBE-C cells showed much higher migration and invasion capabilities than 16HBE cells, and moreover, the suppression of TPD52 by RNAi resulted in significant decrease of migration and invasion capabilities of 16HBE-C cells. These results will be valuable for further investigating and understanding the mechanisms underlying BaP-induced carcinogenesis.

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